Case 1

An EMS notification of prehospital cardiac arrest is received by your community ED. Per the paramedic crew, the patient is a 62-year-old man initially complaining of chest tightness who became unresponsive and apneic during transport approximately 3 minutes prior to arrival. The rhythm was noted initially to be ventricular fibrillation; after a single biphasic countershock, his rhythm became organized, but he remained pulseless. He was intubated en route and is now being wheeled into your critical care area receiving active chest compressions.

You glance at the EMS monitor and note a slow narrow complex rhythm; chest compressions are continued, and his prehospital capnography tubing is connected to the ED monitor. The characteristic waveform reassures you of proper ETT placement, and the ETCO2 is 14 mm Hg. You obtain central access, and a round of ACLS drugs is administered. At the following rhythm check, you note ventricular fibrillation; he receives another shock, and chest compressions continue. You now note an ETCO2 of 36 mm Hg, a central pulse is appreciated, and his plethysmographic waveform becomes clearly defined. Hypothermia is induced, and the patient is admitted to the cardiac critical care unit.

Introduction

Ventilation (the pulmonary exchange of carbon dioxide [CO2] and its subsequent expiration) is typically monitored in the ED by 2 modalities: colorimetric capnometry or continuous infrared spectroscopy. Colorimetric capnometers display a threshold concentration of CO2 qualitatively or semiquantitatively by color change, providing the clinician with confirmation of ETT placement. (See Table 1.) Capnometry by infrared absorbance spectroscopy, on the other hand, allows continuous quantitative assessment of CO2 concentrations displayed by numerical value. Many capnometers also graphically depict the CO2 waveform as a function over time; this capability (known as capnography) provides the clinician with additional information regarding the patient’s ventilatory status. (See Figure 1.) Volumetric capnography, a modality not widely available, plots expired CO2 concentration along with exhaled volume during the respiratory cycle, providing information regarding alveolar and anatomic dead space. This may allow for additional applications, including the bedside diagnosis or exclusion of pulmonary embolism.^1,2

Correlation Of ETCO2 To Arterial CO2

ETCO2 concentration (the concentration of CO2 at the end of exhalation) typically underestimates PaCO2 concentration in healthy individuals by 4 to 5 mm Hg.³ Regrettably, this gap precludes using ETCO2 as a noninvasive determination of PaCO2. The discrepancy between ETCO2 and PaCO2, the so-called “PaCO2-ETCO2 gradient,” is a critical consideration — one that is influenced by 3 primary factors⁴:

• The PaCO2-ETCO2 gradient will be increased in the acute scenario by any disorder that decreases pulmonary blood flow (thereby increasing alveolar dead space). Such conditions include pulmonary embolism, cardiogenic shock, cardiac arrest, or hypovolemia.
• The fixed amount of functional or “anatomic” dead space related to the trachea and other conducting airways also contributes to the gradient.
• Lastly, any condition that decreases exhaled tidal volume, such as obstructive lung disease, increases the gradient. This is due to inadequate expulsion of CO2 contained inside the obstructed alveoli. The amount of such wasted ventilation can be measured using a parameter known as the dead space/tidal volume ratio (VD/VT) or dead space “fraction.”⁷

Thus, the determinants of the PaCO2-ETCO2 gradient are multifactorial, and the magnitude of their effect is often unpredictable. Therefore, while 1the correlation between partial pressure of carbon dioxide in arterial blood (PaCO2) and ETCO2 may be somewhat reliable in stable unintubated ED patients,⁸ it is typically considered unreliable in critically ill patients and may be assumed only with caution.^9-13

Despite pitfalls in using the absolute value of a single ETCO2 reading to gauge PaCO2, it seems intuitive that if the PaCO2-ETCO2 gradient is constant, increases or decreases in ETCO2 on the monitor should reflect those occurring with the PaCO2 in the blood. Disappointingly, however, stability of the PaCO2-ETCO2 gradient is only found to occur in 60% to 80% of patients studied across several anesthesia studies, with the gradient subject to unpredictable amounts of widening or narrowing.⁴ This phenomenon was further demonstrated in a study of multitrauma patients, which found a 27% erroneous prediction of PaCO2 change by ETCO2.¹⁴ One very helpful observation, however, is that the PaCO2-ETCO2 gradient is almost always positive (ie, PaCO2 is nearly always higher than ETCO2), and when a negative gradient exists, it is typically very small. Therefore, while a low ETCO2 value may provide little information regarding a patient’s ventilatory status, a high ETCO2 value almost always correlates with an equal or higher PaCO2 value. This concept may prove particularly beneficial during the continuous monitoring of patients at risk for tiring out, such as those patients with status asthmaticus or decompensated congestive heart failure. Likewise, in situations in which targeted PaCO2 levels may be of value (such as in patients with evidence of increased intracranial pressure and acute brain herniation), a high ETCO2 value may signal the need for adjustments in the patient’s mechanical ventilatory parameters or, at the minimum, the need to check a blood gas.

For healthy patients, the partial pressure of carbon dioxide in venous blood (PvCO2) is commonly acknowledged to be 5 to 8 mm Hg higher than the PaCO2, and in a prospective study of 112 hemodynamically stable ED patients with chronic obstructive pulmonary disease (COPD) exacerbations, arterial hypercarbia was ruled out in all cases where the PvCO2 was found to be below 45 mm Hg.¹⁷ The relationship between PvCO2 and PaCO2 has been shown to be unreliable, however, in critically ill patients with shock states or circulatory failure.¹⁶ In these situations, the PvCO2 becomes significantly elevated as the body buffers the lactic acid being produced. Thus, while it is acceptable to consider low or normal PvCO2 measurements reassuring in patients with respiratory failure, if the PvCO2 is elevated, especially in the context of hypotension, then obtaining an ABG and PaCO2 determination is more appropriate.

ETCO2 Monitoring Applications

Verification Of ETT Placement

Perhaps the most useful application of continuous ETCO2 monitoring is to allow real-time confirmation of adequate ventilation through capnographic waveform analysis. Continuous ETCO2 monitoring is a valuable tool for preventing misplacement of the ETT, either through continuous verification of placement following intubation or for airway management during CPR or transport. This is especially true when one considers the fallibility of traditional physical examination techniques. For instance, auscultation over the chest does not detect up to 15% of esophageal intubations, while fogging in the ETT is reported in up to 85% of esophageal intubations.¹⁸

From the prehospital point of view, esophageal intubations have been reported to range from between 2%¹⁹ to 6%.²⁰ In a study from the Orlando, Florida EMS system, Katz and Falk reported that 27 out of 108 (25%) patients who had a prehospital intubation arrived in the ED with an unrecognized, misplaced ETT: ¹⁸ in the esophagus and 9 above the vocal cords.²¹ However, when ambulances and aeromedical units were equipped with continuous ETCO2 monitors, Silvestri et al reported in a follow-up study that the incidence of unrecognized misplaced ETTs was 0%, compared to the 23% incidence of misplaced ETTs in those units where continuous ETCO2 monitoring was not available.²² Likewise, Grmec et al studied 81 patients (58 with severe TBI) who underwent prehospital intubation and compared auscultation to capnometry with capnography for confirmation of proper ETT placement. Successful intubation was observed in 73 patients; however, 8 patients were intubated into the esophagus – all of which were detected by capnometry. Of those, 4 were incorrectly thought to be in the trachea based upon auscultation.²³ Further emphasizing the importance of accurate determination of ETT placement is Silvestri et al’s study that showed a 69% mortality associated with unrecognized misplaced ETTs and 100% mortality if the patient was apneic upon arrival to the ED.²²

Additionally, the use of continuous ETCO2 in confirming prehospital intubation during cardiac arrest has also been shown to be more effective than colorimetric capnometry and auscultation. The presence of ETCO2 greater than 5 mm Hg after 6 breaths was found to be 100% sensitive and 100% specific for correct placement of the ETT, while qualitative capnometry was 100% specific but only 80% sensitive in cardiac arrest. Both methods were 100% sensitive and 100% specific in non-arrest intubations.²⁴

For emergent, in-hospital intubations, The American College of Emergency Physicians endorses the nearly perfect accuracy of ETCO2 for ETT confirmation but does not differentiate between the utility of qualitative, quantitative, or continuous ETCO2 detectors for the verification or reconfirmation of ETT placement.²⁵ Continuous ETCO2 monitoring from initial ETT placement, and continuing through surgery, is considered standard of care by the American Society of Anesthesiologists to both confirm initial ETT placement and to ensure rapid recognition if extubation were to occur.²⁶

Monitoring During Procedural Sedation

When performing procedural sedation, reliable monitoring of the patient’s ventilatory status is crucial. While clinical indicators like chest rise or the plethysmography-derived respiratory rate provided by electrocardiogram lead placement can be used, monitoring the capnographic waveform for hypopneic and bradypneic hypoventilatory patterns provides the clinician with a quick and more accurate indication of acute respiratory events.²⁷ Burton et al reported that capnographic changes (defined as a change in ETCO2 level greater than 10 mm Hg or intrasedation ETCO2 less than 30 mm Hg or greater than 50 mm Hg) predicted respiratory events by up to 271 seconds.²⁸ Similar findings were observed in a study of 132 patients receiving propofol for conscious sedation in the ED. The results of this randomized controlled study showed that patients monitored by capnography had significantly fewer hypoxic episodes compared to those where the treating physician was blinded to the capnography data. In both groups, all hypoxic episodes were able to be predicted by respiratory depression seen on the capnograph a median of 60 seconds before the onset of hypoxia.²⁹

Often, nasal prongs with an additional port are used to provide continuous CO2 sampling. If commercial devices are not available, a regular nasal cannula can be suitably modified. (See Figure 2.) It is important to note that the CO2 waveform will show ventilatory rate and duration but that the amplitude of the waveform is not a measure of ventilatory depth. Rather, this vertical height of the wave portrays the amount of CO2 being exhaled through the intra-nasal cannula.³⁰ While ETCO2 monitoring for sedation is considered standard of care in the United States in operating suites, its necessity during sedation in the ED is still controversial. ETCO2 monitoring may be most contributory in those patients undergoing preoxygenation and/or oxygen administration during their deep sedation in the ED. In these cases, the continuation of normal oxygen saturation on the pulse oximeter readout can fail to indicate hypoventilation or apnea; this makes ETCO2 monitoring a superior real-time monitoring solution to identify oversedation or apnea in these patients. When ETCO2 monitoring is not available, it may be preferable to withhold supplemental oxygen altogether so that drops in the pulse oximeter reading can be used more reliably as an indicator of hypoventilation and hypercapnea, as was shown in a case series of 513 patients.³⁰ If using pulse oximetry in either situation, knowledge of the lag effect, as described in the “Pulse Oximetry Lag” section, will be important.

Further reading on the use of ETCO2 for procedural sedation can be found in an excellent review written by Krauss and colleagues.²⁷

Monitoring After TBI

Hyperventilation with hypocapnia may worsen outcome in brain-injured patients.¹⁸ Therefore, monitoring of ETCO2 is emerging as a fundamental component of TBI management not only in the hospital but also in the prehospital arena. After TBI, there may be a period of prolonged hypoperfusion with cerebral blood flow (CBF) reduced by as much as two-thirds of normal. Hyperventilation can further decrease CBF, potentially to the point of cerebral ischemia or by converting ischemic areas into infarction. Evidence from in-hospital studies indicates that prophylactic early hyperventilation can seriously compromise cerebral perfusion and worsen patient outcome.³¹ Further, inadvertent hyperventilation during prehospital transport is associated with increased mortality.¹⁸

Several studies have demonstrated the incidence of induced hypocapnia during the field management of TBI patients. In a retrospective study from San Diego, 59 adult severe TBI patients who were unable to be intubated without rapid sequence intubation (RSI) were matched to 177 historical nonintubated controls. The study utilized ETCO2 monitoring and found an association between hypocapnia and mortality and a statistically significant association between ventilatory rate and ETCO2. Both the lowest and final ETCO2 readings were associated with increased mortality versus matched controls. ETCO2 monitoring was used in 144 patients to assess whether closer monitoring would result in a lower rate of inadvertent severe hyperventilation (defined as an ETCO2 less than 25) after RSI. Patients with ETCO2 monitoring had a significantly lower incidence of severe hyperventilation. For those patients who were severely hyperventilated, there was a statistically significant increase in mortality (56% vs 30%).¹⁸ However, as previously discussed, the PaCO2-ETCO2 gradient in traumatically injured patients is unreliable, specifically in regards to low ETCO2 concentrations. A recent study by Lee et al examined 77 patients and showed a poor concordance between ETCO2 and PaCO2 in multitrauma patients.³² Therefore, the reliance on ETCO2 as an indicator of hypocapnia must be further evaluated in the emergency setting before it is used to guide ventilatory management of traumatically brain injured patients in the ED. PaCO2 remains the gold standard.

Prognosis Of Continued CPR

As discussed previously, pulmonary CO2 exchange is affected by multiple factors at the level of the alveoli. In contrast to this, at extremely low flow states, ETCO2 is determined almost entirely by pulmonary flow secondary to a logarithmic relationship between cardiac output and ETCO2 that exists during cardiac arrest.³³ This relationship between pulmonary flow and ETCO2 during arrest makes capnometry an important prognostic marker during CPR in the ED. In multiple studies, an ETCO2 level during CPR of 10 mm Hg or less 20 minutes after the initiation of resuscitation in patients with pulseless electrical activity accurately predicted death in patients suffering prehospital arrest.^34-37 These findings were also supported by a small prospective trial of both in- and out-of-hospital arrest³⁹ and were only minimally affected by variations of ventilatory rate.⁴⁰ However, the initial ETCO2 had no correlation with outcome or survival,³⁴ and very low initial ETCO2 (less than 6 mm Hg) has been associated with survival.⁴⁰ Accordingly, the 2010 Advanced Cardiac Life Support guidelines state, “Persistently low ETCO2 values (less than 10 mm Hg) during CPR in intubated patients suggest that ROSC is unlikely,” and they consider ETCO2 “unreliable immediately after starting CPR.”⁴¹ One caution is that the prognostic value of ETCO2 has not been established in supraglottic airways or in those receiving bag valve mask ventilations.⁴¹ Further, the absence of color change on a colorimetric device is not sufficiently accurate to allow cessation of resuscitation.^41,42 Detection Of ROSC During Cardiac Arrest A sudden rise in ETCO2 during CPR may indicate ROSC. An increase of more than 10 mm Hg from the patient’s baseline should prompt a rhythm check and, if the rhythm is organized, a pulse check.^43-49

Case Conclusion

An ECG of the patient after regaining his pulse revealed ST elevations in the lateral precordial leads. The patient was taken to the cardiac catheterization lab for revascularization on hospital day 1 He was extubated on hospital 1day 2 and optimized on antiplatelet drugs, beta-blockers, and lipid-lowering agents prior to discharge.

ETCO2 Key Points

• Capnography allows for the continuous verification of ETT placement, which is essential in the unstable prehospital and ED environment in which patients are frequently moved; achieving adequate sedation can be difficult, and accidental extubation is an ongoing risk.
• Continuous capnography by spectroscopy may be superior to qualitative CO2 detectors in detecting correct ETT placement during cardiac arrest.
• An ETCO2 less than 10 mm Hg following 20 minutes of CPR is predictive of death and indicates that continued attempts at resuscitation are likely futile.
• A rapid increase in ETCO2 concentration during CPR often represents ROSC and can be a useful guide in determining timing of rhythm and pulse checks.
• Continuous noninvasive ETCO2 monitoring can be useful in the monitoring of patients with tenuous respiratory status, such as those with severe reactive airway disease or congestive heart failure.
• While a low ETCO2 concentration is difficult to interpret, an ETCO2 concentration greater than 40 mm Hg will almost always indicate hypercapnia. The degree of hypercapnia may be underrepresented by the ETCO2.