Capnography in the ED

Author: Zachary Radwine, MD (Senior Resident, UICOMP / OSF St. Francis Medical Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

 

Continuous quantitative waveform capnography, also known as end-tidal carbon dioxide, PetCO2, or ETCO2, is a measurement of the partial pressure of CO2 in the exhaled breath. This technology has been around since the mid-19th century and only relatively recently has its potential in emergency medicine begun to be explored.

Cardiopulmonary Resuscitation

The value of capnography during CPR was recognized as far back as 1987, specifically in a paper by Garnett et al1 showing that end-tidal CO2 (ETCO2) was often the first indicator that return of spontaneous circulation (ROSC) occurred. However it wasn’t until 2010 that the AHA guidelines for CPR included the use of capnography as a Level I recommendation for ET tube verification, Level IIa for detecting ROSC, and Level IIb for monitoring CPR quality2.  This was again stressed in the 2013 AHA consensus statement3, regarding the use of capnography:

  • Most reliable method of confirming and monitoring placement of the ETT (see also Silvestri et al4)
  • Should be primary physiologic metric when neither an arterial nor central line is in place
  • Potential to guide optimization of compression depth and rate and to detect fatigue in the provider performing compressions: consider improving technique or switching provider if ETCO2 <10 mmHg with a goal of >20 mmHg
  • Consider an abrupt sustained increase to a normal value (35-40 mmHg) as an indicator of ROSC
  • Failure to maintain ETCO2>10 mmHg during adult CPR reflects poor cardiac output and strongly predicts unsuccessful resuscitation
  • Avoid unnecessary pulse checks if the level is not compatible with organ perfusion

Heradstveit et al5 published a retrospective study of 575 cardiac arrest patients in 2012. They found that the ETCO2was significantly different in patients with and without ROSC, but depended on the cause of the arrest. Respiratory arrests had higher levels than cardiac, and pulmonary embolism had the lowest levels. For these reasons they concluded it will be difficult to establish a single initial cut-off prognostic value. Also, given the low ETCO2 found in patients later determined to have PE, they postulated that persistently low levels combined with clinical suspicion of PE during ACLS may be an indication for thrombolytics.

A systematic review of 23 observational studies of the prognostic value of ETCO2 in CPR by Touma and Davies6 in 2013 again concluded that no single cut-off value as a predictor of death could be established. However, they said ETCO2 values could be used in conjunction with other prognostic factors and clinical findings to support the decision-making process to terminate CPR.

A prospective study of 80 patients published in 2014 by Akinci et al7 looked at ETCO2  levels after 5,10, 15, and 20 minutes of CPR and showed that levels after 20 minutes to be the most reliable for differentiating patients who will achieve ROSC from those who will not. The best intersection point was 28 mmHg (sensitivity 86%, specificity 80%). No one with level <14 mmHg survived. There was no statistical difference among the presenting rhythms.

The most recent study supporting ETCO2 as a marker of ROSC concluded that a sudden increase of ETCO2 >10 mmHg is likely to indicate ROSC and a pulse check is warranted at this time8. They noted similar findings were shown previously by Grmec et al9. They also noted levels <10 mmHg indicates a very low chance of successful resuscitation, which was also shown previously by Wayne et al10.

Edelson et al11 looked at capnography as a tool for measuring ventilation rate during CPR. They concluded that it was more reliable than standard chest wall impedance algorithms, although both methods tended to underestimate the true rate. This is particularly important as the literature supports the fact that over-ventilation is a common problem despite the AHA recommendation of a respiratory rate of 8-10bpm during ACLS.

To summarize, capnography should be used during CPR to:

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Finally, keep in mind that ETCO2 levels can be transiently affected by administration of both bicarb and pressors.

Septic/Critically Ill Patients

New literature has emerged in the last couple years suggesting a use for capnography in evaluation of septic/critically ill patients. Hunter et al12-13 found that pre-hospital capnography was more predictive of in-hospital mortality than any other vital sign. It was associated with serum bicarbonate, anion gap, and lactate. ETCO2 was significantly lower in those who died. Levels from 31-41 mmHg were considered normal and values outside this range had 93% sensitivity for mortality (specificity 44%, NPV 99%). They also found that in patients with suspected sepsis, there were three independent predictors of mortality:

  1. Use of pressors
  2. Mechanical ventilation
  3. Abnormal ETCO2

They concluded that ETCO2 may perform similarly to lactate as a predictor of mortality in patients with suspected sepsis (excluding patients with COPD and asthma). It is also faster, less invasive, and may reduce time to recognition of the severity of illness.

Another study looked at ETCO2 and volumetric carbon dioxide (VCO2= volume of expired CO2) as predictors of fluid responsiveness in hemodynamically unstable patients14. They determined either of these parameters could be used as an indicator of fluid responsiveness following a preload challenge. However, absolute changes in ETCO2 were small and thus VCO2 may be more useful.

Other proposed uses for capnography include monitoring of patients with DKA, recognition of respiratory failure in seizing and post-ictal patients, and monitoring response to treatment of CHF, COPD, and asthma15.

Pulmonary Embolism

The potential role of dead space ventilation in the evaluation of PE was proposed back in 1959. PE creates dead space, which is then translated as a drop in alveolar and thus end-tidal carbon dioxide.  The dead space can then be calculated using arterial CO2 and ETCO2. A meta-analysis16 of 14 trials found that when all the data was pooled, the overall sensitivity and specificity was 0.8 and 0.49, respectively. Due to heterogeneity and variation in measurement techniques (some used dead space as an end-point while others used ETCO2) they were unable to calculate an optimal diagnostic threshold. They concluded that capnography might permit the exclusion of PE in cases in which the pre-test probability is <10%.

One trial17 in the meta-analysis found that an ETCO2 ≥ 36 mmHg, when combined with a Well’s score ≤ 4, had a NPV of 97.6%.

Another trial18 found a statistically significant difference in ETCO2 in patients with and without PE. However, they also concluded that the sensitivity is not sufficient to rule out PE, but may help reduce unnecessary testing when combined with D-dimer and other scoring systems.

Procedural Sedation and Analgesia

The current literature regarding use of capnography for procedural sedation and analgesia (PSA) in the ED can be summed up by the 2014 ACEP policies subcommittee on PSA statement 19:

“Although the routine use of capnography appears to decrease the incidence of hypoxia and respiratory events as defined in these studies (Level B recommendation), currently there is a lack of evidence that capnography reduces the incidence of serious adverse events during procedural sedation and analgesia such as neurologic injury caused by hypoxia, aspiration, or death. Future studies should focus on these areas to provide a better understanding of these outcomes.”

For further reading refer to studies by van Loon20, Deitch21, and Waugh22. Also see the pro and con editorial in Annals of Emergency Medicine June 201323.

Sources // Further Reading

  1. Garnett AR, et al. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. JAMA. 1987 Vol 257(4):512-15.
  2. Neumar R, Otto C, Link M, et al. Part 8: adult advanced cardiovascular life support: 2010 American heart association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2010;122:S729-S767.
  3. Meaney PA, et al. Cardiopulmonary Resuscitation Quality: Improving cardiac outcomes both inside and outside the hospital: a consensus statement for the American Heart Association. Circulation. 2013;128:417-35.
  4. Silvestri S, Ralls GA, Krauss B, et al. The effectiveness of out-of-hospital use of continuous end-tidal carbon dioxide monitoring on the rate of unrecognized misplaced intubation within a regional emergency medical services system. Ann Emerg Med. 2005;45:497.
  5. Heradstveit BE, et al. Factors complicating interpretation of capnography during advanced life support in cardiac arrest- a clinical retrospective study in 575 patients. Resuscitation. 2012 Jul;83(7):813-8.
  6. Touma O, Davies M. The prognostic value of end tidal carbon dioxide during cardiac arrest: a systematic review. Resuscitation. 2013;84:1470-79.
  7. Akinci E. Comparison of end-tidal carbon dioxide levels with cardiopulmonary resuscitation. Pak J Med Sci. 2014;30(1):16-21.
  8. Pokorna M, et al. A sudden increase in partial pressure end-tidal carbon dioxide (Petco2) at the moment of return of spontaneous circulation. J Emerg Med. 2010;38(5):614-21.
  9. Grmec S, Klemen P. Does the end-tidal carbon dioxide (EtCO2) concentration have prognostic value during out-of-hospital cardiac arrest? Eur J Emerg Med. 2001;8:263–9.
  10. Wayne MA, Levine RL, Miller CC. Use of end-tidal carbon dioxide to predict outcome in prehospital cardiac arrest. Ann Emerg Med. 1995;25:762–7.
  11. Edelson D, et al. Capnography and chest-wall impedance algorithms for ventilation detection during cardiopulmonary resuscitation. Resuscitation. 2010;81:317-22.
  12. Hunter C, et al. The sixth vital sign: prehospital carbon dioxide predicts in hospital mortality and metabolic disturbances. Am J Emerg Med. 2014;32:160-65.
  13. Hunter C, et al. End-tidal carbon dioxide is associated with mortality and lactate in patients with suspected sepsis. Am J Emerg Med. 2013;31:64-71.
  14. Young A, Marik P, et al. Changes in end-tidal carbon dioxide and volumetric carbon dioxide as predictors of volume responsiveness in hemodynamically unstable patients. Journal of Cardiothoracic and Vascular Anesthesia. 2013;27(4):681-84.
  15. Manifold C, et al. Capnography for the nonintubated patient in the emergency setting. J Emerg Med. 2013 May;45(4):626-32.
  16. Manara A, et al. Capnography as a diagnostic tool for pulmonary embolism: a meta-analysis. Ann Emerg Med. 2013;62:584-91.
  17. Hemnes AR, et al. Bedside end-tidal CO2 tension as a screening tool to exclude pulmonary embolism. Eur Resp J. 2010;35:735-41.
  18. Kurt OK, et al. The diagnostic role of capnography in pulmonary embolism. Am J Emerg Med. 2010 Vol 28:460-65.
  19. Godwin SA, Burton JH, Gerardo CJ, et al. Clinical policy: procedural sedation and analgesia in the emergency department. Ann Emerg Med. 2014;63:247-258.
  20. van Loon K, et al. Capnography during deep sedation with proposal by nonanesthesiologists: a randomized controlled trial. Anesthesia Analgesia. 2014 Jul;119(1):49-55.
  21. Deitch K, et al. Does end tidal CO2 monitoring during emergency department procedural sedation and analgesia with proposal decrease the incidence of hypoxic events? a randomized, controlled trial. Ann Emerg Med. 2010;55(3):258-64.
  22. Waugh J, et al. Capnography enhances surveillance of respiratory events during procedural sedation: a meta-analysis. J Clin Anes. 2011;23:189-96.
  23. Mohr N, Wessman B, Terp S, Schriger D. Routine capnography in procedural sedation. Ann Emerg Med. 2013;61(6):697-99.
  24. Nolan J. High-quality cardiopulmonary resuscitation. Curr Opin Crit Care. 2014;20:227-223.
  25.  Nolan J. Airway management in cardiopulmonary resuscitation. Curr Opin Crit Care. 2013;19:181-87.
  26.  Grmec S, Kupnik D. Does the Mainz Emergency Evaluation Scoring (MEES) in combination with capnometry (MEESc) help in the prognosis of outcome from cardiopulmonary resuscitation in a prehospital setting? Resuscitation. 2003;58:89–96.
  27. Kartal M, et al. ETCO2: a predictive tool for excluding metabolic disturbances in nonintubated patients. Am J Emerg Med. 2011;29(1):65-69.
  28. http://www.ncbi.nlm.nih.gov/pubmed/24560835
  29. http://www.ncbi.nlm.nih.gov/pubmed/22929141
  30. http://www.ncbi.nlm.nih.gov/pubmed/24986960
Edited by Alex Koyfman, MD

7 thoughts on “Capnography in the ED”

  1. Very nice post, thx!

    One comment: I find your first paragraph a bit misguiding. Continuous capnography is so much more than ETco2 especially in the intubated patient which I’m sure you agree. Much can be derived from the waveform. As an introduction to the uninitiated these two handbooks seem to cover the most basic waveforms. They seem ok even if provided by industry. I have no involvement whatsoever, just found them by quick search.

    Carefusion: http://www.carefusion.com/pdf/Center_for_Safety/Documents/RC1706-L3017-Capnography-Handbook.final.pdf

    Philips:
    http://bcrt.ca/wp-content/uploads/2010/09/capnography_quickguide.pdf

    All the best
    Mads

  2. Very nice post, thx!

    One comment: I find your first paragraph a bit misguiding. Continuous capnography is so much more than ETco2 especially in the intubated patient which I’m sure you agree. Much can be derived from the waveform. As an introduction to the uninitiated these two handbooks seem to cover the most basic waveforms. They seem ok even if provided by industry. I have no involvement whatsoever, just found them by quick search.

    Carefusion: http://www.carefusion.com/pdf/Center_for_Safety/Documents/RC1706-L3017-Capnography-Handbook.final.pdf

    Philips:
    http://bcrt.ca/wp-content/uploads/2010/09/capnography_quickguide.pdf

    All the best
    Mads

  3. Great Review thanks, I’ve been meaning to read up on this again for ages! I think it should be used to help inform our gestalt rather than than being too binary about it.

    Just a wee note for any UK FOAMers out there (cos I can never remember):
    35- 45 mmHg = 4.66- 5.9
    20mmHg = 2.66
    10mmHg = 1.33

    I think I’ll (try) and keep 1.3 and 2.5 in my head as useful reference points.

    BTW theres a nice/brief summary of the physiology behind it on Anaesthesia UK – http://www.frca.co.uk/article.aspx?articleid=100389

    Thanks again!

  4. Great Review thanks, I’ve been meaning to read up on this again for ages! I think it should be used to help inform our gestalt rather than than being too binary about it.

    Just a wee note for any UK FOAMers out there (cos I can never remember):
    35- 45 mmHg = 4.66- 5.9
    20mmHg = 2.66
    10mmHg = 1.33

    I think I’ll (try) and keep 1.3 and 2.5 in my head as useful reference points.

    BTW theres a nice/brief summary of the physiology behind it on Anaesthesia UK – http://www.frca.co.uk/article.aspx?articleid=100389

    Thanks again!

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