End Tidal Capnography in the Emergency Department

The EtCO₂ level may help guide decision-making in assessing whether continued resuscitation in cardiac arrest is futile. Values <10 mm Hg after 20 minutes of active resuscitation have consistently demonstrated minimal chance of survival.^17,25,26 In one study, an EtCO₂ of <10 mm Hg at 20 minutes had a sensitivity, specificity, PPV, and NPV of 100% for death in PEA arrest.¹⁷ However, determination of the specific EtCO₂ cutoff and the timing is still an area of research with a final consensus pending.^17,18,25-30 One recent study suggested that even 3 min with EtCO₂ <10 mm Hg could be an appropriate cutoff to cease resuscitation efforts.²⁷

Unfortunately, there is a large amount of heterogeneity in the available literature using capnography to assess for ROSC and in guiding resuscitation efforts. EtCO₂ should not be used as the only factor in the determination to cease resuscitation. In addition, the AHA recommends that EtCO₂ for prognostication should be limited to intubated patients only.²⁰

It is important to note that while cardiac output is the largest factor for EtCO₂ in arrest, other physiologic and iatrogenic causes may affect EtCO₂ during resuscitation. For example, there is considerable variation in EtCO₂ with changes in ventilation rate.⁴ Measured CO₂ may be significantly lower with manual instead of mechanical ventilation, likely due to over-ventilation that not only reduces alveolar CO₂ but also causes excess intra-thoracic pressure, reducing venous return.²¹ For these reasons, use caution when using EtCO₂ during manual ventilation of an intubated patient in cardiac arrest. In addition, administration of epinephrine may cause a small decrease in EtCO₂, although the effect may vary for each individual.^10,31 Sodium bicarbonate can also cause a transient increase in CO₂ due to its conversion into CO₂ and H₂O.¹⁰

Procedural Sedation

Capnography is being used with increasing frequency to monitor patients during procedural sedation; it is now considered standard of care in many settings.³² Although rare, hypoventilation is a risk of procedural sedation.³³ Typically, respiratory depression during procedural sedation is diagnosed with non-invasive pulse oximetry and visual inspection.³⁴ However, capnography has been shown to identify respiratory depression, airway obstruction, apnea, and laryngospasm earlier than pulse oximetry, allowing the provider to intervene quicker.^34,35 Unlike pulse oximetry, the capnogram also remains stable during patient motion and is reliable in low-perfusion states.³⁶

There are two distinct types of hypoventilation detected by capnography. Bradypneic hypoventilation (type 1), which is characterized by a decreased respiratory rate, results in a decreased expiratory time and a subsequent rise in EtCO₂.³⁶ This is depicted on capnography by a high EtCO₂ and longer waveform, and is commonly observed after oversedation with opioids (Figure 4).³⁶ In contrast, hypopneic hypoventilation (type 2) occurs with low tidal volumes but a normal respiratory rate.³⁶ Type 2 is graphically represented by a suddenly lower ETCO₂ with otherwise normal waveform and occurs most commonly with sedative-hypnotic drugs (Figure 5).³⁶ Seeing either type during procedural sedation should alert the clinician to assess for airway obstruction, consider supplemental oxygen, cease drug administration or reduce dosing, and consider reversal if appropriate.³⁶