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Designed, Produced, and maintained (Edition 10, March 2019) by 

Bhavani Shankar Kodali MD

This is another capnogram which may not be an infrequent occurrence

 

 

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.

 

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What happens to PETCO2 when there is pneumothorax?

   I have been asked this question by several colleagues. The answer, however, is not simple. It depends on the status of a pneumothorax (evolution), cause of pneumothorax, and the content of the pneumothorax (air/oxygen/nitrous oxide versus carbon dioxide). Pneumothorax can affect the PETCO2 as well as the shape of the capnograms. 

 

  If the pneumothorax is progressing towards a tension pneumothorax, then obviously the PETCO2 will decrease due to decreases in cardiac output.

 

 

 

 

If a pnemothorax is small, one may not find any difference, and therefore it is non-diagnostic. However, as the pneumothrorax increases in size, the changes in capnography depend on the tidal volume delivered which is  a function of the mode of ventilation, i.e., 'pressure controlled' versus 'volume controlled'.  If pressure controlled, then tidal volume will decrease, resulting in a gradual increase in the PaCO2 and PETCO2 as well (hypoventilation). However, the PETCO2 may decrease due to inadequate sampling of alveolar CO2 due to the tidal volume becoming progressively smaller. Moreover, as tension pneumothorax increases in size,  thereby decreasing cardiac output, PETCO2 decreases.  A volume controlled ventilation is more likely to increase intra-thoracic pressure with increasing pnuemothorax which imposes a mechanical impedance to the circulation and results in a decrease in PETCO2.1

 

If the cause of pneumothorax is due to an obstruction to exhalation,  an obstructive capnogram (prolonged phase II and increased slope of Phase III) with increasing PETCO2 can be observed.  In a case report by Smith et al,1 a normal capnogram changed to an obstructive picture in 45 minutes, following the induction of general anesthesia and IPPV. Ventilation was increased to offset increasing PETCO2. Ten minutes later, circulatory collapse occurred with decreasing end-tidal PCO2 to 15 mm Hg. Examination of the chest revealed bilateral tension pneumothorax.  Although capnography was being used continuously, the altered CO2 waveform that occured went unrecognized. The authors retrospectively felt that important diagnostic clue could have led the authors to search for and correct the cause of expiratory obstruction very early in the evolution of this event. The cause of the pneumothorax was a defective bacterial filter of the breathing circuit.

 

An obstructive pattern on a capnogram has been reported when a patient developed pneumothorax during laparoscopic Nissen fundoplication.2 There was also an increase in peak inspiratory pressures and wheezing was also noted on ascultation. Several puffs of albuterol nebulizations were administered which resulted in a cessation of the wheezing. However, the obstructive pattern on the capnogram persisted. There was a gradual decrease in the oxygen saturation towards the conclusion of the surgery. A postoperative X-ray revealed a 100% left-sided pneumothorax.  

 

 

 

 

The obstructive pattern on the capnogram is probably due to compression of the airways by the pneumothorax.

 

Reports of characteristic changes of the descending limb can be found in the literature. A staircase  effect on the descending limb of the capnogram is seen in the presence of  a pneumothorax in neonates.3,4 When chest tubes are correctly positioned, a staircase effect may indicate chest tube occlusion.3

 

 

 

 

Carbon dioxide pneumothorax:Capnopneumothorax

 

When pneumothorax occurs as a complication of CO2 induced pneumoperitoneum, it results in an increase in the PETCO2.5-9 This could be an early warning sign of CO2 pnuemothorax when associated with increases in the peak inspiratory pressure. In one study, PETCO2 and PaCO2 increased in all patients who developed CO2 pneumothorax,  and ventilation was increased to offset increases in PETCO2.5 However, no changes in CO2 waveform were observed in this study. In a retrospective of 968 laparoscopic surgical cases, PETCO2 greater than 50 mm Hg and operative times greater than 200 minutes were predictors of  the development of pneumothorax and/or pneumomediastinum.9 

 

 

 

 

If pneumothorax is not diagnosed and it progresses into a tension pneumothorax, then it may result in a decrease in PETCO2 secondary to circulatory collapse.

 

 

 

 

 

1.    Smith EC, Otworth JR, Kaluszyk, P.  Bilateral tension pneumothorax due to a defective anesthesia breathing circuit filter.  J Clin Anesth 1991;3:229-234.

 

2.    Manger D, Kirchhoff GT, Leal JJ, Laborde R, Fu E.  Pneumothorax during laparoscopic Nissen fundoplication.

 

3.    Smalhout B, Kalenda Z. An Atlas of Capnography. Kerckebosche Zeist.The Neterhlands. 2n ed. 1981:163.

 

4.    Curley MAQ, Thompson JE.  End-tidal CO2 monitoring in critically ill infants and children.  Pediatric Nursing 1990;16;397-403.

 

5.    Joris JL, Chiche JD,Lamy ML. Pneumothorax during laproscopic fundoplication: diagnosis and treatment with positive end-expiratory pressure. Anesth Analg 1995;81:993-1000.

 

6.    Perke G, Fernandez A.  Subcutaneous emphysema and pneumothorax during laparoscopy for ectopic pregnancy removal. Acta Annesthesiol Scan 1997;41(6):792-4.

 

7.    Peden CJ, Prys-Roberts C.  Capnothorax: implications for the anaesthetist. Anaesthesia 1993;48:664-6.

 

8.    Chui PT, Gin T, Chung SC.  Subcutaneous emphysema, pneumomediastinum and pneumothorax complicating laparoscopic vagotomy. Anaesthesia 1993;48(11):978-81.

 

9.    Murdock CM,Wolff AJ, Van GeemT.  Risk factors for hypercarbia, subcutaneous emphysema, pneumothorax, and pneumomediastinum during laparoscopy. Obstet Gynecol 2000;95:704-9.

 

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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

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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

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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.

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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.

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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.

Reference:

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.

 

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Cardiac output and PETCO2

   During steady-state gas exchange equilibrium, the alveolar PCO2 (PACO2), tissue CO2 production (VCO2), and alveolar ventilation (VA) are related as given by the following equation: 

 

PACO2 = (K)VCO2/VA

 

   During constant ventilation and CO2 production, an abrupt reduction in cardiac output  (Qt) reduces PECO2.1-7 This may occur because of two mechanisms.1,2

 

(1) A reduction in venous return causes a decrease in CO2 delivered to the alveolar compartment, resulting in decreased PACO2. The percent decrease in PETCO2 is directly correlated with the percent decrease in cardiac output (slope= 0.33, r2=0.82 in 24 patients undergoing aortic aneurysm surgery with constant ventilation).1  Also, the percent decrease in CO2 elimination is similarly correlated with the percent decrease in cardiac output (slope=0.33, r2=0.84).1 The changes in PETCTO2 and CO2 elimination following hemodynamic perturbation were parallel. These findings suggest that decrease in PETCO2 quantitatively reflect the decreases in CO2 elimination.1

 

(2) An increase in alveolar dead space, which results from the decreased pulmonary vascular pressure, will dilute the CO2 from normally perfused alveolar spaces to decrease PETCO2 below PACO2. 

 

During sustained reduction in cardiac output, however, increasing CO2 accumulation in the peripheral tissues and venous blood will begin, after 10-20 min, to restore CO2 delivery to the lungs and PETCO2 toward baseline levels. 

 

Reciprocal changes in PETCO2 will occur during acute increases in CO2. Increases in cardiac output and pulmonary blood flow result in better perfusion of the alveoli and a rise in PETCO2.3,4 Consequently alveolar dead space is reduced as is (a-ET)C02 The decrease in (a-ET)PC02 is due to an increase in the alveolar C02 with a relatively unchanged arterial C02 concentration, suggesting better excretion of C02 into the lungs. The improved C02 excretion is due to better perfusion of upper parts of the lung.2   The relationship between PETCO2 and pulmonary artery blood flow was studied during separation from cardiopulmonary bypass.5 This showed that PETCO2 is a useful index of pulmonary blood flow. A PETCO2 greater than 30 mm Hg was invariably associated with a cardiac output more than 4 L/min or a cardiac index > 2 L/min.5 Furthermore, when PETCO2 exceeded 34 mm Hg, pulmonary blood flow was more than 5 L/min (CI > 2.5 L).5

 

Thus, under conditions of constant lung ventilation, PETCO2 monitoring can be used as a monitor of pulmonary blood flow.2,5-8  

 

Recently, using Fick's Principle, attempts were made to determine cardiac output non-invasively implementing periods of CO2 rebreathing during which CO2 partial pressure of oxygenated mixed venous blood is obtained from the measured exponential rise of the PETCO2 value. In addition, oxygen uptake, carbon dioxide elimination, end-tidal PCO2, oxygen saturation, and tidal volume were  determined. These results are encouraging in patients with healthy lungs.9  Whereas the results are considered controversial when the lungs are diseased.10

 

References:

 

1   Shibutani K, Muraoka M, Shirasaki S, Kabul K, Sanchala VT, Gupte P.  Do changes in end-tidal PCO2 quantitatively reflect changes in cardiac output? Anesth Analg 1994;79:829-33.

 

2    Isserles SA, Breen PH.  Can changes in end-tidal PCO2 measure changes in cardiac output? Anesth Analg 1991;73:808-14.

 

3   Leigh MD, Jones JC, Motley HL. The expired carbon dioxide as a continuous guide of the pulmonary and circulatory systems during anesthesia and surgery.  J Thoracic cardiovasc surg 1961;41:597-610.

 

4    Askrog V.  Changes in  (a-A)CO2 difference and pulmonary artery pressure in anesthetized man. J Appl Physiol 1966;;21:1299-1305.

 

5   Maslow A, Stearns G, Bert A, Feng W, Price D, Schwartz C, Mackinnon S, Rotenberg F, Hopkins R, Cooper G, Singh A, Loring SH. Monitoring end-tidal carbon dioxide during weaning from cardiopulmonary bypass in patients without significant lung disease. Anesth Analg 2001;92:306-13.

 

6   Weil MH, Bisera J, Trevino RP, Rackow EC.  Cardiac output and end-tidal carbon dioxide. Crit Care Med 1985;13:907-9.

 

7   Ornato JP, Garnett AR, Glauser FL.  Relationship between cardiac output and the end-tidal carbon dioxide tension.  Ann Emerg Med 1990;19:1104-6.

 

8  Jin X, Weil MH, Povoas H, Pernat A, Xie J, Bisera J.  End-tidal carbon dioxide as a noninvasive indicator of cardiac index during circulatory shock. Crit care Med 2000;28:2415-9.

 

9.    Gedeon A, Krill P, Kristensen J, Gottlieb I. Noninvasive cardiac output determined with a new method based on gas exchange measurements and carbon dioxide rebreathing: A study in animals/pigs. J Clin Monit 1992;8:267-78.

 

10.    Pianosi P, Hochman J. End-tidal estimates of arterial PCO2 for cardiac output measurements by CO2 rebreathing: a study in patients with cystic fibrosis and healthy controls. Pedatr Pulmonol 1996;22:154-60.

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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
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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

References:

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.

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