Carbon Dioxide Narcosis Due to Inappropriate Oxygen Delivery

A Case Report

Thomas Herren; Eva Achermann; Thomas Hegi; Adrian Reber; Max Stäubli

Disclosures

J Med Case Reports. 2017;11(204) 

In This Article

Case Presentation

A 72-year-old, cachectic (height 170 cm, weight 50 kg, BMI 17.3 kg/m2) Caucasian man with COPD and a history of smoking had increasing shortness of breath. Pulmonary function testing performed 9 years prior showed a decreased forced expiratory volume in 1 second (FEV1) [38% of predicted, Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 3], which did not increase after albuterol inhalation. The high total lung capacity and residual volume were consistent with emphysema. On arrival of the emergency medical team at his home, our patient was dyspneic but alert. His vital signs were: blood pressure 150/100 mmHg, heart rate 103 bpm, and SpO2 81%. High-flow O2 was supplied at 10 L/min. using a non-rebreathing mask with an O2 reservoir bag (Fig. 1). The SpO2 increased to 99% within 20 minutes, and our patient was transported to the emergency department. As it was unknown whether our patient had a hypoxic respiratory drive, O2 flow was erroneously limited to 4 L/min. He got increasingly irritated, had no headache, but was no longer oriented to time, place, and person, and became unconscious, gasping for air 2 hours later. His blood pressure was 110/80 mmHg, and the heart rate was 80 bpm. Breath sounds were distant, and his tongue was cyanotic. An arterial blood gas analysis taken shortly after starting bag-valve-mask ventilation showed marked hypercapnia with respiratory acidosis (Table 1A). Noninvasive ventilation was not a possible option.[6] Our patient was intubated, mechanically ventilated, and received albuterol and ipratropium bromide by inhalation. Methylprednisolone, amoxicillin clavulante plus clarithromycin (for an infiltrate in the right paracardiac region), and low-dose theophylline were administered intravenously. Four hours later, our patient was extubated (Table 1B), and was later transferred to a medical ward. The high PaCO2 was explained by low tidal volumes and a probably hypoxic ventilatory drive (Table 1C). Because of our patient's worsening dyspnea, he mistakenly received O2 at 2 L/min. by the same non-rebreathing mask (Fig. 1). After a few hours, intensive care unit (ICU) admission was required due to hypotension (75/50 mmHg) and bradypnea (Table 1D). He was re-intubated and mechanically ventilated for 24 hours. Norepinephrine was given to stabilize the blood pressure. An electrocardiogram (ECG) showed a sinus rhythm with right bundle branch block and right ventricular hypertrophy, and the echocardiography documented a chronic cor pulmonale with pulmonary arterial hypertension. Respiratory acidosis improved, and the patient was temporarily extubated (Table 1E). However, aspiration of a pea (removed by bronchoscopy, Fig. 2) with atelectasis of the right lung again necessitated mechanical ventilation and a tracheostomy. One month after admission, the exhausted patient died of CO2 narcosis (Table 1F). An autopsy was not performed.

Figure 1.

Photograph of a non-rebreathing mask with an oxygen reservoir bag attached. The mask has one unidirectional inspiration valve and two unidirectional expiration valves. The carbon dioxide exhaled by the patient is constantly diluted by a high flow of oxygen delivered to the mask (10–15 L/min.)

Figure 2.

Photograph made during bronchoscopy on day 10. A pea is visible in the bronchus to the right laterobasal pulmonary segment

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