Carbon Dioxide Detector

Anatomy and Physiology

Waveforms

The graph demonstrates a typical CO₂ waveform that might be seen from a mainstream capnograph (see Graph. CO₂ Waveform). Phase A represents the first exhalation step as gas from the dead space arrives at the detector. This dead space gas contains no CO₂ introduced from the lungs and, therefore, is seen as a flat, zero concentration of CO₂ over time. Phase B demonstrates the rapid rise in CO₂ as the expiratory phase continues and the concentration of CO₂ rises. This phase reflects a mixing of the dead space gas, which lacks CO₂, and the alveolar gas. Phase C represents the alveolar plateau phase, where the concentration of CO₂ becomes more constant over time. The rate of rise of this phase can change in certain pathological states, for example, with bronchospasm, where the rise is steeper. Point D represents the “end-tidal CO₂” level; this is the highest concentration of CO₂ during the cycle and occurs at the end of expiration. Phase E shows the rapid decline in CO₂ concentration that begins with inspiration as external gas enters the lungs. This external gas has a low concentration of CO₂, and the waveform returns to baseline.

Alterations to this typical waveform can be used as clues that alert the clinician to changes in the status of their patient. Hyperventilation typically produces a pattern of increased respiratory frequency associated with a depressed waveform. Hypoventilation is known to occur in at least 2 common types. A decreased respiratory rate causes Bradypnea hypoventilation and produces a waveform pattern with low respiratory frequency and elevated ETCO₂. Hypopneic hypoventilation, in contrast, reveals a decreased ETCO₂ caused by the patient taking shallower breaths than normal. Although these are both forms of hypoventilation, 1 results in an elevation of ETCO₂, and the other causes a decrease in ETCO₂.

Clinical Significance

Procedural Sedation and Analgesia

Continuous end-tidal CO₂ monitoring during the performance of procedural sedation and analgesia (PSA), sometimes called “conscious sedation,” is often recommended as a measure to detect respiratory depression. The medications associated with PSA, such as proposal, benzodiazepines, and narcotics, can often lead to respiratory depression. It is essential to recognize that the levels of sedation represent a continuum of drug effects. The lightest forms of sedation include mild anxiolysis, where a patient can generally respond after receiving these medications. At the other extreme is deep sedation or general anesthesia, where the patient requires active respiratory support and may require hemodynamic support during the procedure. PSA is intended to preserve a patient’s basic cardiopulmonary functioning; however, the medications used in PSA can have side effects, including hypotension, loss of protective airway reflexes, and hypoventilation. Respiratory depression is considered to be 1 of the most significant risks during the administration of PSA. To address the risk of hypoventilation, many experts who study and provide PSA have explored whether CO₂ monitoring can help identify hypoventilation and improve patient safety. Oxygen saturation has classically been used as the marker for hypoventilation. However, this may be a late marker of hypoventilation, particularly when supplemental oxygen is administered prophylactically during the administration of PSA.

Some specialty societies whose members perform PSA have recommendations about CO₂ monitoring.[2] The American Society for Anesthesia promotes stronger recommendations about CO₂ monitoring during moderate and deep sedation while others have less proscriptive suggestions about its use.[3][4][3] Adoption of the practice of regular CO₂ monitoring during PSA has been less rapid for those providers outside of the operating room due to limitations in evidence to support objective benefits and the lack of available equipment and training.[5] Furthermore, the clinical relevance is still being evaluated.[6] Other groups, such as a recent Cochrane review, have argued that the current evidence is not able to demonstrate a difference in outcomes when using CO₂ monitoring in addition to standard monitoring.[7]

Endotracheal Tube Confirmation and Monitoring

CO₂ detection has grown to be used as an important indicator to confirm the correct placement of an endotracheal tube (ETT) after intubation. Airway experts widely recommend this as a required step in ETT confirmation.[8] Capnography has been shown to be a highly reliable method of endotracheal tube confirmation. A properly positioned tube in the trachea produces a reliable CO₂ waveform that can be detected reliably by these sensors. Esophageal intubation does not transmit CO₂ to the detector and would indicate improper placement. Hypopharyngeal intubation is a special circumstance when the endotracheal tube is not positioned through the vocal cords, but rather just superior to the glottis. Hypopharyngeal intubations can be difficult to identify clinically, and capnography may assist in detecting this situation through an abnormal or inconsistent waveform. Additional methods of confirming tube position include direct visualization of the glottis, auscultation for breath sounds and inspection for chest rise during ventilation.

A false negative CO₂ reading may occur in cases of cardiac arrest when there is no cardiopulmonary circulation to carry CO₂ to the alveoli and, ultimately, to the detector. In this case, it is possible that an endotracheal tube could be properly positioned in the trachea yet not provide a CO₂ waveform. However, the detector does not produce a waveform with ventilation and could lead to the wrong conclusion. Early initiation of CPR during cardiac arrest leads to circulatory flow which can then generate aO₂2 waveform, helping confirm proper tube position. In the later phases of resuscitation as cell death occurs, even with CPR being performed, the CO₂ levels fall.

Continuous CO₂ monitoring of an intubated patient can also help identify accidental endotracheal tube displaced during transport or movement of a patient. Continuous monitoring can also help detect other post-intubation complications such as airway obstruction from a kinked ETT or mucous plugging. Anytime a waveform is suddenly lost, it should alert the clinician to evaluate the equipment and connections and determine if there is a more concerning cause for the loss.

Cardio Pulmonary Resuscitation (CPR)

Effectiveness of CPR

Immediately after a cardiac arrest and during CPR, chest compressions generate cardiac output that results in circulatory flow and the generation of a CO2 waveform. In cardiac arrest without compressions, there may be no detectable CO₂ level. End-tidal CO₂ levels correlate with the effectiveness of the compressions and can be used to help guide resuscitation.[9] High-quality CPR produces higher cardiac output and, therefore, higher CO₂ levels than poor-quality CPR.  This information can guide the resuscitation. Important factors that lead to high-quality CPR include rate, depth, recoil and the lack of interruptions. These factors should be assessed when there is a low CO2 level during the resuscitation of a patient with cardiac arrest. Compressor fatigue can lead to loss of quality compressions and can be detected by a decline in end-tidal CO₂ levels. Cardiac arrest teams can give feedback to the compressor about their technique, or they may choose alternate to a “fresh” compressors based on these levels. The American Heart Association 2010 recommendations suggest that an ETCO₂ level of less than 10 mm Hg during CPR would be a reasonable indication to aim efforts toward improving the quality of compressions.

Return of Spontaneous Circulation

During cardiac arrest, when there is a triumphant return of spontaneous circulation (ROSC), there is an associated rise in end-tidal CO2 levels; this is often the first sign of ROSC.[10] A sudden rise in CO2 may alert the cardiac arrest team that there is ROSC and trigger an assessment of circulatory status through pulse, rhythm, and blood pressure. The clinical relevance is to avoid unnecessary interruptions in CPR. A rise in CO₂ may be an earlier sign of ROSC than performing frequent pulse checks that cause a pause in compressions.

Termination of Resuscitation

End-tidal CO₂ is also helpful during resuscitation to help predict death after a prolonged cardiac arrest. After 20 minutes of CPR, an end-tidal CO₂ level of 19 mm Hg or less is predictive of death as an outcome of the cardiac arrest.[11] It can be challenging to make the clinical decision when to terminate resuscitative efforts when caring for a patient experiencing cardiac arrest. ETCO₂ levels provide additional data to the clinician to help make this decision.[12]

Future and Growing Applications

ETCO₂ approximates the arterial concentration of CO₂ (PaCO₂).  It is typically 2 to 5 mm Hg lower and can be used to estimate the effectiveness of ventilation. This gap can be affected by multiple disease states such as asthma, COPD, pneumonia, pulmonary embolism among others that cause a change in V/Q mismatching, alteration of physiological dead space or shunt physiology. CO₂ detection provides a window into ventilation, pulmonary perfusion, and cardiac output.  Multiple disease states are being studied in attempts to find clinical correlations to CO₂ levels. Recent work has explored various possible uses, including determination of metabolic rate, diagnosis of pulmonary embolism, and assessment for diabetic ketoacidosis.[13][14][15] As equipment becomes more available, novel uses of capnography are being studied and the relationship between end-tidal carbon dioxide and CPR quality during both in-hospital and out-of-hospital cardiac arrest.

Enhancing Healthcare Team Outcomes

Nurses, respiratory therapists, and clinicians must be aware of the pitfalls and considerations when using CO₂ detectors. an interprofessional team approach to monitoring patients using these devices produces the best patient outcomes.