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End Tidal CO2
Nicholas McManus

Nicholas McManus

Is End Tidal CO2 the real 6th vital sign?

End-Tidal CO2 is an under-utilized and frequently overlooked modality for monitoring patients in the Emergency Department. Here is why you should pay close attention to it...
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End-Tidal CO2 (etCO2) is an under-utilized and frequently overlooked modality for monitoring patients in the Emergency Department. A normal value is 35-45 mmHg. If I had my way, it would be a mandatory reportable vital sign on all critically ill patients. Let me show you why…

The presence of a normal capnogram denotes a patent airway and spontaneous breathing, and normal ETco2 levels indicate adequate ventilation and perfusion

But first, what does that waveform even mean?

Simply put…as the patient breaths out, the graph goes up and as the patient breaths in, the graph goes down.

But why can't I just use pulse oximetry?

Key points on Pulse Oximetry

    • Large changes in the SaO2 occur with small changes in the PaO2.
    • Pulse oximeters are generally accurate between 80% and 100%.
    • At levels < 80%, large changes in PaO2 occur with small changes in SaO2.
    • SaO2 values at or below 96% have been shown to be 100% sensitive for detection of hypoxia (PaO2< 70).

Pulse oximetry also has significant limitations….

    • Tells you nothing about pH
    • Tells you nothing about PaCO2
    • Tells you nothing about ventilation

Capnography (etCO2) = measurement of CO2 during Expiration

  • etCO2 is usually 2 to 5 mmHg < PaCO2 due to the dilution of the end-tidal gases by physiologic dead space gas.
  • VQ mismatch ratios including pulmonary embolism, cardiac arrest, hypovolemia and obstructive lung disease can all widen the Pa-etCO2 gradient

Clinical uses for etCO2 (evidence to follow)

    • Provide qualitative and quantitative methods of assessing cardiac output
    • Monitor effectiveness of CPR
    • Determine prognosis of out-of-hospital cardiac arrest
    • Confirm ETT placement in the trachea (gold standard)
    • Continuously monitor ETT position
    • Monitoring for over-sedation during procedural sedation and analgesia
    • Assess response to treatment in patients with acute respiratory distress
    • Assist with differentiating pulmonary edema/CHF from asthma/COPD
    • Maintain appropriate etCO2 levels in patients with elevated intracranial pressure
    • Estimate PaCO2 in patients with normal lung function
    • Determine adequacy of ventilation in patients with altered mental status
    • Assess ventilatory status of actively seizing patients – the only modality that can
    • Assess metabolic acidosis

etCO2 during CPR

Measured etCO2 is determined by lung ventilation and perfusion. In the intubated patient, assuming there are no complications with the ventilatory circuit, ventilation is kept quite constant. So, any changes in etCO2 are the direct result of sudden changes in perfusion. In a patient in cardiac arrest, perfusion is dependent entirely on cardiac output. Therefore, we can indirectly use etCO2 as a marker of sudden changes in cardiac output. How does this information help us improve the quality of CPR?

Effectiveness of compressions

In studies, etCO2 has been shown to be a reliable indicator of effective compressions.1,2,3 A decrease in etCO2 suggest a decrease in cardiac output. This may be due to compressor fatigue or occlusion of the left ventricular outflow tract. If the etCO2 is less than 10, improve compressions by switching out compressors or changing the location of hand placement on the chest.

Return of Spontaneous Circulation (ROSC)

Changes in etCO2 is often the first clinical indicator that ROSC has occurred and may be seen even before your next pulse check.3 During CPR, if you see a sudden and sustained increase in etCO2, check for a pulse. 

Prognosis of CPR success

Measurements of etCO2 can be used to accurately predict non-survival of patients with cardiopulmonary arrest.

Cantineau 19964

    • Prospective study of 87 patients presenting in asystole
    • An etCO2 < 10 at 20 minutes after endotracheal intubation provided an observed sensitivity of 100% in predicting return of spontaneous circulation

Callaham, 19905

    • Prospective study of 55 adult, nontraumatic prehospital cardiac arrest patients
    • Patients who developed a pulse had a mean etCO2 of 19 at the start of resuscitation, and those who did not had a mean etCO2 of 5 (p less than .0001)
    • An initial PetCO2 of 15 correctly predicted eventual return of pulse with a sensitivity of 71%, specificity of 98%, a positive predictive value of 91%, and a negative predictive value of 91%

Levine, 19976

    • Prospective observational study in 150 patient who sustained out-of-hospital cardiac arrest presenting in pulseless electrical activity
    • Average etCO2 in non-survivors at 20 minutes was 4.4
    • Average etCO2 in survivors at 20 minutes was 32.8
    • The sensitivity, specificity, positive predictive value, and negative predictive value were all 100 percent.

Ahrens, 20017

    • 127 patients in cardiac arrest
    • All but 1 patient with an etCO2 < 10 mmHg died prior to hospital discharge while an etCO2 >10 mmHg were associated with various degrees of survival

Bottom Line:

    • If the etCO2 is < 10 mmHg, 20 minutes after endotracheal intubation, literature suggests continued resuscitation efforts will most certainly be futile
    • If the etCO2 is > 20 mmHg, 20 minutes after endotracheal intubation, literature suggests a possible chance of survival to hospital discharge and continued resuscitation efforts may be warranted depending on clinical circumstances.

Despite this knowledge, less than 50% of hospitals are using etCO2 to determine CPR effectiveness and less than 8% are using etCO2 to prognosticate survivability.8

But, consider this...IV Epinephrine may affect etCO2 readings

Cantineau, 19949

  • Prospective study of 20 patients in who sustained out-of-hospital asystolic cardiac arrest.
  • etCO2 was measured before and 3 minutes after peripheral intravenous (IV) injection of 2 mg epinephrine. No other resuscitative drugs were administered during the study period.
  • Mean etCO2 decreased from 16.7 +/- 9.3 mm Hg before epinephrine to 12.6 +/- 7.1 mm Hg after epinephrine. The mean change in etCO2 was 4.15 +/- 3.5 mm Hg (P < .0001).
  • Four patients had ROSC and the decrease in etCO2was similar between the patients who had ROSC and those who did not.

Sodium Bicarbonate administration may also play a factor

Okamoto, 199510

  • IV NaHCO3 forms excess CO2 resulting in an immediate increase in measured etCO2
  • This study took 15 anesthetized dogs and injected then with NaHCO3
  • etCO2 increased for 5 to 10 minutes following administration. 

Confirmation of endotracheal tube placement

Waveform capnography is considered the most reliable method to confirm endotracheal tube placement in emergency conditions in the prehospital setting with a Sensitivity and Specificity of 100%.11 With esophageal intubation, no or small transient waveforms will be seen (see associated photo). Colorimetric etCO2 is a reliable alternative when waveform capnography is not available, but this can be falsely positive in patients who have recently consumed carbonated beverages or antacids and those with prolonged ventilation by bag-valve mask. If colorimetric etCO2 is used, it is most accurate after 6 breaths and false positives can be minimized by waiting this duration prior to connecting the colorimetric monitor.12

During CPR, a sudden loss of waveform suggests an issue with the ventilatory circuit. Check the endotracheal tube for dislodgment, disconnection or other equipment malfunction.

Procedural Sedation

Capnography provides an earlier warning of respiratory depression and airway compromise earlier than pulse oximetry when monitoring during moderate sedation.13,14 In a randomized controlled trial of 132 Emergency Department patients undergoing procedural sedation with Propofol, hypoxic events were identified up to 240 seconds before identification by pulse oximetry.15 etCO2 has a clear benefit at decreasing the incidence of over-sedation and serious adverse events and should always be used if available.

Asthma/COPD

Can etCO2 measurements accurately predict arterial PaCO2?

Corbo, 200515

    • Prospective observational cohort study of adult asthmatic patients presenting with an acute exacerbation
    • etCO2 correlates with measured PaCO2 levels with a mean difference of 1 mmHg (95% CI -0.1 – 2 mmHg)

Cinar, 201216

    • Prospective observational study of 162 patients presenting to the ED with acute dyspnea
    • Mean etCO2 level was 39.47 ± 10.84 mmHg and mean PaCO2 level was 38.95 ± 12.27 mm Hg
    • 80% of the etCO2 measurements were between the range of ± 5 mm Hg.
    • There was a statistically significant correlation between etCO2 and PaCO2 (r = 0.911, P < .001).

Doğan NÖ ŞA, 201417

    • 102 patients presenting with an acute COPD exacerbation
    • Pre-treatment and post-treatment etCO2 levels were assessed in comparison to PaCO2 levels
    • etCO2 positively correlated with arterial partial carbon dioxide pressure levels
      • Pre-treatment (r= 0.756, P < .001)
      • Post-treatment (r= 0.629, P < .001)

While measurement of etCO2 doesn’t substitute for the amount of information a complete arterial blood gas provides, it may be useful in assessing dynamic response to therapy in these patients.

With obstructive lung patterns as seen in Asthma, COPD or bronchospasm, a “shark fin” appearance to the waveform is seen due to loss of alveolar plateau with prolonged expiration. 

Pulmonary Embolism

Can etCO2 be used to rule out clinically significant pulmonary embolism?

Hemnes, 201018

    • 298 patients enrolled over 6 months at a single academic center
    • etCO2 was measured within 24 hours of contrast-enhanced computed tomography, lower extremity duplex or ventilation/perfusion scan
    • 13% of patients were diagnosed with PE (this is interesting in itself)
    • Results
      • Healthy control group etCO2: 36.3 ± 2.8
      • Non-PE group etCO2: 35.5 ± 6.8
      • PE group etCO2: 30.5 ± 5.5 (p < 0.001)
    • An etCO2 > 36 mmHg had a Sensitivity of 87 and a Specificity of 53, a negative predictive value of 96.6%.
    • The negative predictive value increased to 97.6% when combined with a Wells score < 4

While this may look promising, a prospective trial in comparison to D-dimer would be nice to see.

Can etCO2 predict patients who have subclinical PE's?

In pulmonary embolism, etCO2 is decreased secondary to a reduction in lung perfusion and an increase in alveolar dead space ventilation, resulting in less etCO2 being exhaled from the lungs.20 However, the amount of measurable arterial CO2 from the ABG will remain unchanged. This results in an increase in the etCO2 gradient (PaCO2 – etCO2). Normal being within 2-5 mmHg. In a prospective review of surgical patients undergoing anesthesia, three asymptomatic patients were identified with a pulmonary embolism after being found to have an elevated etCO2 gradient (17-27 mmHg).21

Can etCO2 be used for monitoring patient improvement during thrombolysis?

Two case reports of patients requiring thrombolysis for pulmonary embolism were described. etCO2 was measured before, during and after thrombolysis. Late dead-space fraction was measured and decreased in the two patients from 64.4% to 1.1% and from 25.6% to 5.7% after thrombolysis, with a concomitant resolution of right heart dysfunction on echocardiogram.22

Congestive Heart Failure (CHF)

The symptoms of cardiac versus respiratory causes of dyspnea overlap, and rapid differentiation of the underlying etiology can sometimes be challenging.

Can etCO2 be used to differentiate heart failure from acute asthma/COPD?

Brown, 199823

    • Prospective observational study of 42 patients presenting to the ED with acute dyspnea
    • Results
      • CHF/Pulmonary Edema etCO2: 27.1 ± 7.8
      • Asthma/COPD etCO2: 33.4 ± 9.6
    • However, no single etCO2 level was found to be a reasonable predictor of diagnosis

Grmec, 200724

    • Prospective study from January 2005 to June 2006 comparing etCO2 measurements in patients presenting with acute dyspnea from pulmonary edema/CHF versus asthma/COPD
    • Results
      • CHF/Pulmonary Edema etCO2: 28.5 ± 8.2
      • Asthma/COPD etCO2: 48.0 ± 8.2

Klemen, 200925

    • Prospective study of 441 patients presenting to the ED with acute dyspnea
    • Results
      • CHF/Pulmonary Edema etCO2: 28.5 ± 8.2
      • Asthma/COPD etCO2: 43.5 ± 9.7
    • etCO2 < 40 mmHg was a strong independent predictor for acute HF

An etCO2 level > 37 mmHg was not observed in any patient with heart failure, although ETC02 level > 37 mmHg has a slight sensitivity for diagnosis of COPD/asthma.

Trauma

Can etCO2 predict the need for massive transfusion?

Stone, 201726

    • 67 patients included (49% blunt force trauma)
    • Set to determine if measured etCO2 on arrival predicted the need for massive transfusion within the first 6 hours, defined as the need of ≥ 3 units of packed red blood cells per hour
    • Isolated head injuries, traumatic arrests, or pre-hospital intubations were excluded
    • etCO2 < 35 was found to be an independent predictor for the need of massive transfusion. (OR 9.24, 95% CI 1.51-56.57, p=0.016).

Can etCO2 predict mortality in trauma?

Childress, 201827

    • Retrospective, cross-sectional study of 135 trauma patients transported by a single EMS agency to a level one trauma center
    • Set out to evaluate the association of prehospital EtCO2and in-hospital mortality in trauma patients
    • Results
      • Non-survivors mean etCO2: 18 mmHg (95% CI 9-28)
      • Survivors mean etCO2: 34 mmHg (95% CI 32-35)
    • etCO2 < 30 mmHg had a sensitivity of 89%, specificity of 68%, PPV of 13% and NPV of 99% for predicting mortality.
    • There was no correlation between respiratory rate and etCO2 (correlation 0.16; p = 0.06)

I would like to take this time to reflect on my initial argument suggesting etCO2 should be a measured vital sign. Implementation of etCO2 as a measured vital sign mayimprove triage and assist EMS in directing patients to an appropriate trauma center.

Diabetic Ketoacidosis

Patients with diabetic ketoacidosis (DKA) hyperventilate, which lowers alveolar and arterial carbon dioxide levels. Because etCO2 closely approximates PaCO2, measured etCO2 levels may allow for clinical prediction of patients in DKA.

Can etCO2 be used to rule out DKA in hyperglycemic patients?

Fearon, 200228

    • Cross sectional, prospective observational study of 42 children presenting to a pediatric emergency department with suspected DKA
    • Results
      • Children without DKA etCO2: 37 mmHg (95% CI = 35.5 to 37.9)
      • Children with DKA etCO2: 22 mmHg (95% CI = 17.4 to 26.9)
    • An etCO2 < 29 mmHg correctly classified 95% of children with DKA, with a sensitivity of 83% and a specificity of 100%
    • No patient with an etCO2of > 36 mmHg had DKA, for a sensitivity of 100% (95% CI = 0.74 to 1.0)

Soleimanpour, 201329

    • Cross-sectional prospective descriptive-analytic study of 181 ED patients older than 18 years old with blood sugar levels of higher than 250 mg/dl and probable DKA.
    • ABG and capnography were obtained from all patients.
    • etCO2 > 24.5 mmHg accurately ruled out the DKA with a sensitivity and specificity of 90%

Chebl, 201630

    • Cross sectional observational study of 71 adults ≥ 17 years of age presenting to the ED 2014 with glucose > 550 mg/dL
    • The area under the curve for etCO2 was 0.95 (95% CI of 0.91 to 0.99)
    • Sensitivity for DKA at etCO2 ≥ 35 mmHg was 100% (95 % CI, 83.9-100)
    • Specificity for DKA at etCO2 level ≤ 21 mmHg was 100% (95 % CI, 92.9-100.0)

While these findings are quite interesting, etCO2 should not be used as a substitute for true blood gases in the workup of Diabetic Ketoacidosis as this is still the gold standard.

Conclusion

Despite the vast amount of supporting literature, etCO2 remains an under-utilized and frequently overlooked modality for monitoring patients in the Emergency Department. As clinicians, we look for noninvasive and rapid indicators to assist with diagnosis, risk stratification and to assess response to treatment. etCO2 is widely available, easy to use apply and easy to interpret. If you take nothing else from this topic, please focus on the benefits of etCO2 in the resuscitation of patients in cardiac arrest and I recommend implementation of this in your practice, if you have not already.

References

  1. Ornato JP GE, Garnett AR, et al. Effect of cardiopulmonary resuscitation compression rate on end-tidal carbon dioxide concentration and arterial pressure in man.Crit Care Med. 1988;16:241–5. [PubMed] 
  2. Falk JL RE, Weil MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation.N Engl J Med. 1989;318:607–11. [PubMed] 
  3. Garnett AR OJ, Gonzalez ER, Johnson EB. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. 1987;257:512–5. [PubMed] 
  4. Cantineau JP, et al. End-tidal carbon dioxide during cardiopulmonary resuscitation in humans presenting mostly with asystole: A predictor of outcome.Crit Care Med. 1996;24:791–6. [PubMed] 
  5. Callaham M BC. Prediction of outcome of cardiopulmonary resuscitation from end-tidal carbon dioxide concentration.Crit Care Med. 1990;18:358–62. [PubMed] 
  6. Levine RL WM, Miller CC. End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest.N Engl J Med. 1997;337:301–6. [PubMed] 
  7. Ahrens T ea. End-tidal carbon dioxide measurements as a prognostic indicator of outcome in cardiac arrest. Am J Crit Care. 2001;10:391–8.[PubMed] 
  8. Turle S SP, Nicholson S, et al. Availability and use of capnography for in-hospital cardiac arrests in the United Kingdom. 2015 ;94:80–4. [PubMed] 
  9. Cantineau JP MP, Lambert Y, et al. Effect of epinephrine on end-tidal carbon dioxide pressure during prehospital cardiopulmonary resuscitation.Am J Emerg Med. 1994;12:267–70. [PubMed] 
  10. Okamoto H HS, Kawasaki T, et al. Changes in end-tidal carbon dioxide tension following sodium bicarbonate administration: Correlation with cardiac output and haemoglobin concentration.Acta Anaesthesiol Scand. 1995;39:79–84. [PubMed] 
  11. Š G. Comparison of three different methods to confirm tracheal tube placement in emergency intubation. Intensive Care Med. 2002;28:701–4.[PubMed] 
  12. Garnett AR GC, Gervin AS. Capnographic waveforms in esophageal intubation: Effect of carbonated beverages.Ann Emerg Med. 1989;18:387–90. [PubMed] 
  13. Adams L BS, Spurlock D Jr. Capnography (ETCO2), respiratory depression, and nursing interventions in moderately sedated adults undergoing transesophageal echocardiography (TEE) J Perianesth Nurs. 2015 ;30(1):14–22.[PubMed] 
  14. Burton JH HJ, Germann CA, Dillon DC. Does end-tidal carbon dioxide monitoring detect respiratory events prior to current sedation monitoring practices?Acad Emerg Med. 2006;13:500–504. [PubMed] 
  15. Deitch K MJ, Chudnofsky CR, et al. Does end tidal CO2 monitoring during emergency department procedural sedation and analgesia with propofol decrease the incidence of hypoxic events? A randomized, controlled trial.Ann Emerg Med. 2010;55:258–264. [PubMed] 
  16. Corbo J BP, Lahn M, et al. Concordance between capnography and arterial blood gas measurements of carbon dioxide in acute asthma. Ann Emerg Med. 2005;46:323–327. [PubMed] 
  17. Cinar O AY, Arziman I, et al. Can mainstream end-tidal carbon dioxide measurement accurately predict the arterial carbon dioxide level of patients with acute dyspnea in ED. Am J Emerg Med. 2012;30:358–361. [PubMed] 
  18. Doğan NÖ ŞA, Günaydın GP, et al. The accuracy of mainstream end-tidal carbon dioxide levels to predict the severity of chronic obstructive pulmonary disease exacerbations presented to the ED.Am J Emerg Med. 2014 ;32(5):408–11. [PubMed] 
  19. Hemnes AR NA, Rosenbaum B, Barrett TW, Zhou C, Rice TW, Newman JH. Bedside end tidal CO2 as a screening tool to exclude pulmonary embolism. Eur Respir J. 2010;35(4):735–41.[PubMed] 
  20. Aminiahidashi H, Shafiee S, et al. Applications of End-Tidal Carbon Dioxide (ETCO2) Monitoring in Emergency Department: A Narrative Review. Emerg (Tehran). 2018;6(1):e5
  21. Taniguchi S IK, Sakaguchi Y, et al. Capnometry as a tool to unmask silent pulmonary embolism.Tohoku J Exp Med. 1997;183(4):263–71. [PubMed] 
  22. Verschuren F HE, Clause D, et al. Volumetric capnography as a bedside monitoring of thrombolysis in major pulmonary embolism.Intensive Care Med. 2004 ;30(11):2129–32. [PubMed] 
  23. Brown LH GJ, Seim RH. Can quantitative capnometry differentiate between cardiac and obstructive causes of respiratory distress? Chest. 1998;113(2):323–6. [PubMed] 
  24. Grmec Š GM, Klemen P, Cander D. Utility of the quantitative capnometry (QC) and rapid bedside test for N-terminal pro-brain natriuretic peptide (pro-BNP) in the evaluation of respiratory distress in prehospital setting – preliminary results. J Emerg Med. 2007;33(3):322.
  25. Klemen P GM, Grmec S. Combination of quantitative capnometry, N-terminal pro-brain natriuretic peptide, and clinical assessment in differentiating acute heart failure from pulmonary disease as cause of acute dyspnea in pre-hospital emergency setting: study of diagnostic accuracy.Croat Med J. 2009 50(2):133–42. [PubMed] 
  26. Stone ME, Kalata S, et al. End-tidal CO 2 on admission is associated with hemorrhagic shock and predicts the need for massive transfusion as defined by the critical administration threshold: A pilot study. 2017;48(1):51–7. [PubMed] 
  27. Childress K, Arnold K, et al. Prehospital End-tidal Carbon Dioxide Predicts Mortality in Trauma Patients.Prehospital Emergency Care. 2017:1–5. [PubMed] 
  28. Fearon DM SD. End-tidal carbon dioxide predicts the presence and severity of acidosis in children with diabetes. Acad Emerg Med. 2002 (12):1373–8.[PubMed] 
  29. Soleimanpour H TA, Niafar M, et al. Predictive value of capnography for suspected diabetic ketoacidosis in the emergency department.West J Emerg Med. 2013;14(6):590–4. [PubMed]
  30. Chebl RB, Madden B, et al. Diagnostic value of end tidal capnography in patients with hyperglycemia in the emergency department.BMC emergency medicine. 2016;16(1) [PubMed] 
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