Uncommon cause of increased end-tidal carbon dioxide during endoscopic retrograde cholangiopancreatography under sedation

Dear Editor,

Inadequate oxygenation and ventilation remain as one of the leading causes of morbidity associated with procedural sedation. During sedation, respiratory depression is diagnosed by assessing the respiratory rate, effort, depth of breathing, and end-tidal carbon dioxide (EtCO₂) levels. Hypopnoea often precedes oxygen desaturation in this context. Hence, continuous monitoring of EtCO₂ is essential for the early detection of respiratory compromise.[1]

A common practice during upper gastrointestinal endoscopy is insufflation of the digestive tract with carbon dioxide (CO₂) to enhance visualisation of the mucosal lining. CO₂ is preferred over air by the endoscopists due to its rapid absorption in the gastrointestinal (GI) tract, which significantly reduces post-procedural abdominal pain, bloating, and the risk of air embolism.[2,3,4] The absorbed CO₂ is subsequently eliminated via the lungs. However, reflux of CO₂ from the upper GI tract into the airway may also occur, leading to falsely elevated EtCO₂ readings [Figure 1]. As these procedures are often performed under sedation, such elevations can be misinterpreted as respiratory depression, potentially resulting in unnecessary interventions.

Figure 1.

High end-tidal carbon dioxide values recorded during carbon dioxide insufflation (1a shows 225 mmHg, 1b shows 161 mmHg) during endoscopic retrograde cholangiopancreatography

We report an observation during upper GI endoscopy performed under sedation in a 71-year-old female weighing 59 kg, who was a known case of portal biliopathy. After transferring to the operating theatre, standard American Society of Anesthesiologists (ASA) monitors were attached, including pulse oximeter, non-invasive blood pressure, electrocardiogram, and side-stream capnometer. For the measurement of EtCO₂, a sampling line was connected to an infant feeding tube (10 French, 52 cm) (Amigo Surgicare Pvt. Ltd., India), which was trimmed to 5 cm and inserted into the patient’s nasal cavity. In the prone position, sedation was initiated with an intravenous bolus of ketamine 1 mg/kg, followed by a continuous infusion of propofol at 100 µg/kg/min via an infusion pump (INfusia SP7s, Fresenius Kabi AG, Germany). Respiratory parameters, including respiratory rate, chest rise, oxygen saturation, and EtCO₂, were continuously monitored. During the procedure, an abrupt spike in EtCO₂ to 225 mmHg was noted [Figure 1a]. This sudden increase in EtCO₂ alarmed us. A quick troubleshooting of the various causes was done, and hypoventilation was ruled out as the patient’s respiratory rate, chest movements, and oxygen saturation remained within normal limits. The possibility of a faulty monitor was ruled out, as it was calibrated, and a proper trace was obtained. As the fraction of inspired carbon dioxide (FiCO₂) had increased, we thought of the possibility of extraneous addition of CO₂. When we notified this concern to the endoscopist, they informed us that they had insufflated CO₂. This was identified as the cause of the abrupt rise in EtCO₂ over 225 mmHg [Figure 1a]. Over 8 minutes, we noted a decline in EtCO₂ to 161 mmHg [Figure 1b]. Although CO₂ was elevated to extremes, there was no change in haemodynamics (oxygen saturation: 99%, non-invasive blood pressure: 168/97 mmHg, heart rate: 83/min) [Figure 1a]. During this time, the fraction of inspired CO₂ had increased transiently to 20 mmHg, implying passive reflux of CO₂ from the gastrointestinal tract to the upper airway.

Though this increase in EtCO₂ is transient, we need to be cautious, especially in patients with glaucoma, coronary artery disease, and chronic obstructive pulmonary disease. Hypercapnia leads to cerebral and ocular vasodilation and raises intraocular pressure in glaucoma patients. In coronary artery disease patients, it may cause arrhythmias, decreased myocardial contractility, and increased sympathetic stimulation (tachycardia, hypertension), leading to further worsening of myocardial ischaemia. Acute-on-chronic hypercapnia in chronic obstructive pulmonary disease can lead to CO₂ narcosis, headache, confusion, lethargy, and respiratory failure.

This case underscores the importance of interdisciplinary communication during procedures involving sedation and endoscopy. Awareness of CO₂ insufflation and its potential impact on EtCO₂ readings is essential to prevent unnecessary alarms and to ensure patient safety. This phenomenon is benign, requires no specific intervention, and typically resolves once CO₂ insufflation is discontinued. Key distinguishing features include an abrupt rise in EtCO₂, often exceeding 75 mmHg while the patient’s respiratory rate and depth remain within normal limits.

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Authors contributions

RCN: manuscript preparation, editing, literature search, and conduct of cases. CRT: Concepts, Design, Definition of intellectual content, manuscript preparation, editing, review and approval. SAS: Definition of intellectual content, literature search, conduct of cases, manuscript preparation, editing, review and approval.

Supplementary material

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Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.