The following is an excerpt from the book Emergency Capnography. This volume was written to bridge the gap between the overly brief descriptions of capnography in the textbooks and overly detailed and dense journal literature. The author found that putting his monitor on a wooden chair under bright lights while playing good medic/bad medic did not make it reveal its secrets.
The author, Hugh Greenbaum, is a paramedic and EMS educator with Forest View Volunteer Rescue Squad in Richmond, VA. He has more than 39 years of volunteer EMS experience.
MAJOR TRAUMA
Studies indicate that arterial CO2 measurements (PaCO2) may be significantly higher than ETCO2 measurements in severe trauma patients. This is caused by both the decrease in venous return to the lungs and the gradual depletion of bicarbonate stores. The result is that the low ETCO2 may lead a provider to hypoventilate the patient to raise the ETCO2, which leads to an artificially induced respiratory acidosis. These studies also indicate that acidosis is a predictor of poor patient outcomes. While our goal is to achieve ETCO2 measurements in the range of 30–35 mmHg, we must ensure that proper oxygenation and ventilation are maintained throughout the shock/trauma resuscitation efforts.1,2,3
The recommended ETCO2 range (30–35 mmHg) is based on two factors. First, this range is appropriate for head-injured patients, and many of our trauma patients also have traumatic brain injuries. Second, as PaCO2 may be significantly higher than ETCO2, maintaining the patient in the recommended range keeps the patient within a normal to high range, thus minimizing or preventing respiratory acidosis.
TRAUMATIC BRAIN INJURY
Traumatic brain injury patients suffer from two related and competing problems. The injury results in cerebral swelling and edema, which reduces cerebral blood flow. Hyperventilation (ETCO2 measurements below 30 mmHg) will reduce the swelling but will also reduce cerebral blood flow. Hypoventilation (ETCO2 measurements above 40 mmHg) will increase cerebral blood flow but also increase swelling. The challenge then is to balance these two potentially lethal sequelae. Maintaining ETCO2 between 30 and 35 mmHg balances the need to reduce swelling with the need to retain cerebral blood flow3.
The brain injury itself can complicate the situation. Bradypnea, as part of Cushing’s Triad, can lead to respiratory acidosis. These patients may require artificial ventilations to support adequate ETCO2 and SpO2 values. On the other hand, the patient’s injury may result in tachypnea, resulting in respiratory alkalosis. It may be necessary to paralyze and mechanically ventilate these patients.
Another complication is that studies have demonstrated that the correlation between ETCO2 and PaCO2 measurements is poor in patients with traumatic brain injuries.4 PaCO2 is higher, often significantly, than ETCO2. The significance of this finding is that withholding ventilations to raise the ETCO2 to 30 mmHg is both unnecessary (PaCO2 is near normal) and dangerous for the patient because oxygenation is not being maintained. Similarly, allowing ETCO2 measurements greater than 35 mmHg means the patient’s PaCO2 is in a very unhealthy range (well above normal). These patients should be ventilated at a rate at the high end of normal.
Another way to use capnography to support the head injured patient is to combine ETCO2 trend with mean arterial pressure (MAP) trend. If both MAP and ETCO2 are trending downward, the patient is losing critical perfusion and needs fluid support to maintain sufficient pressure to prevent cerebral ischemia.5
BURNS
As with trauma and head injured patients, the correspondence between ETCO2 and PaCO2 in burn patients is poor.1 The goal of ventilation, just as with trauma and traumatic brain injury, is to ensure adequate oxygenation (SpO2 ≥ 94%), not simply to maintain ETCO2 within the textbook range.
PAIN MANAGEMENT
It is tempting to use capnography, along with cardiac monitoring, to judge the degree of a patient’s pain. A patient in pain may be expected to be tachycardic and to have hypercarbia due to increased metabolism from both the pain itself and the precipitating insult. The patient may also be tachypneic from either (or both) pain caused by ventilations or from CO2 build-up. The problem with this approach is many medical problems cause tachycardia, hypercarbia, and tachypnea, thus confounding any findings. Tachycardia and abnormal capnography must be assumed to be related to the patient’s medical condition and not the patient’s degree of pain.
Similarly, a patient who is normocardic and normocapnic may still be experiencing considerable pain. Isolated extremity injuries can be quite painful, but the degree of sympathetic nervous system stimulation will vary between individuals.
Thus, capnography cannot be used to objectively determine a patient’s level of pain.
However, capnography plays a crucial role in managing the use of pain medications that can cause central nervous system depression (e.g., narcotics, benzodiazepines), respiratory depression, and/or respiratory arrest. Capnography can detect and alarm respiratory changes much faster than human observation or pulse oximetry. By observing trends in the ETCO2 measurements and ventilation rate, supplemented by low ventilation alarms, the provider can obtain early warning of medication-induced hypoventilation or apnea. This gives the provider time to adjust, or reverse, the medication prior to the patient becoming apneic.6,7,8,9
Capnography can be used to help patients manage their pain when medication is contraindicated or ineffective through biofeedback. This must be explained to the patients that they need to either (or both) reduce their ventilatory rate or increase their ETCO2 measurement. In many cases, the patients are able to adjust their ventilations, which improves their status.10,11 At the very least, this may distract the patient from their discomfort, which may improve their ventilatory status.
REFERENCES
1. Cooper, C. J., Kraatz, J. J., Kubiak, D. S., Kessel, J. W., & Barnes, S. L. (2013). Utility of prehospital quantitative end tidal CO2? Prehospital and Disaster Medicine, 28(2), 87–93. https://doi.org/10.1017/S1049023X12001768
2. Doppmann, P., Meuli, L., Sollid, S. J. M., Filipovic, M., Knapp, J., Exadaktylos, A., Albrecht, R., & Pietsch, U. (2021). End-tidal to arterial carbon dioxide gradient is associated with increased mortality in patients with traumatic brain injury: A retrospective observational study. Scientific Reports, 11(1), 1–9. https://doi.org/10.1038/s41598-021-89913-x
3. Frakes, M. A. (2011). Capnography during transport of patients (inter/intra-hospital). In J. S. Gravenstein, M. B. Jaffe, N. Gravenstein, & D. A. Paulus (Eds.), Capnography (2nd ed.). Cambridge University Press.
4. Yang, J. T., Erickson, S. L., Killien, E. Y., Mills, B., Lele, A. v., & Vavilala, M. S. (2019). Agreement between arterial carbon dioxide levels with end-tidal carbon dioxide levels and associated factors in children hospitalized with traumatic brain injury. JAMA Network Open, 2(8), 1–12. https://doi.org/10.1001/jamanetworkopen.2019.9448
5. Grayson, K. (2016). Capnography in the patient with severe neurological injury. EMS1. https://www.ems1.com/ems-products/capnography/articles/capnography-in-the-patient-with-severe-neurological-injury-5ksMR7FvD9Fgp9b3/
6. Burton, J. H., Harrah, J. D., Germann, C. A., & Dillon, D. C. (2006). Does end-tidal carbon dioxide monitoring detect respiratory events prior to current sedation monitoring practices? Academic Emergency Medicine, 13(5), 500–504. https://doi.org/10.1197/J.AEM.2005.12.017
7. Hatlestad, D. (2005). Capnography in sedation and pain management. Emergency Medical Services, 34(3), 65–69.
8. Hutchison, R. (2006). Capnography monitoring during opioid PCA administration. Journal of Opioid Management, 2(4), 207–208. https://doi.org/10.5055/jom.2006.0032
9. Krauss, B., & Hess, D. R. (2007). Capnography for procedural sedation and analgesia in the emergency department. Annals of Emergency Medicine, 50(2), 172–181. https://doi.org/10.1016/j.annemergmed.2006.10.016
10. Meckley, A. (2009). Balancing Unbalanced Breathing: The Clinical Use of Capnographic Biofeedback. 41(4), 183–187. https://doi.org/10.5298/1081-5937-41.4.02
11. Meuret, A. E. (2011). Biofeedback. In J. S. Gravenstein, M. B. Jaffee, N. Gravenstein, & D. A. Paulus (Eds.), Capnography (2nd ed.). Cambridge University Press.
