Carbon dioxide poisoning: a literature review of an often forgotten cause of intoxication in the emergency department

Tests performed on mongrel dogs show the physiological effect of carbon dioxide on the body: after inhalation of a 50% CO₂ and 50% air mixture, respiratory movement increased for about 2 min, and then, it decreased for 30–90 min. Hill and Flack showed that CO₂ concentrations up to 35% have an exciting effect upon both circulation and respiration, but those beyond 35% are depressant upon them [6, 14]. The blood pressure (BP) decreased transiently during the increased respiratory movement and then rose again and maintained the original level for a while. The heart rate slowed slightly just after the gas mixture inhalation. It is believed that the initial BP depression with the decreased heart rate is due to the direct depressant effect of CO₂ upon the heart and that the return of blood pressure to its original level was due to the rapid rise of PaCO₂. After 30–90 min, the respiratory center was depressed, and hypotension occurred gradually or suddenly from reduced cardiac output, leading to an apnea and eventually to circulatory arrest [6].

In higher concentrations of CO₂, unconsciousness occurred almost instantaneously and respiratory movement ceased in 1 min. After a few minutes of apnea, circulatory arrest was seen. These findings show that the cause of death in breathing high concentrations of CO₂ is not the hypoxia but the intoxication of carbon dioxide [6].

Carbon dioxide at low concentration has little, if any, toxicological effects. At higher concentrations (>5%), it causes the development of hypercapnia and respiratory acidosis. Severe acidosis increases the effects of parasympathetic nervous activity, possibly by interfering the hydrolysis of acetylcholine by acetylcholinesterase, resulting in a depression of the respiration and the circulation [6]. Concentrations of more than 10% carbon dioxide may cause convulsions, coma, and death [1, 15]. CO₂ levels of more than 30% act rapidly leading to loss of consciousness in seconds. This would explain why victims of accidental intoxications often do not act to resolve the situation (open a door, etc.) [7, 10, 16].

Studies have shown a wide variability of CO₂ tolerance. Blood concentrations ranged between at least 0.055 and 0.085 atm. (41.8–64.6 mmHg) among subjects with symptoms, suggesting that a safe CO₂ exposure level cannot be characterized by a single value [10]. Concentrations of fatal cases of carbon dioxide vary between 14.1 and 26% CO₂ and an accompanying O₂ level between 4.2 and 25% [1, 8, 11]. It was also determined that CO₂ tolerance decreases with age (p < 0.0001) and suggested that smokers might have more tolerance due to habituation of higher CO₂ levels in cigarette smoke [10, 16].

Effects of oxygen treatment have been studied on animal models, and both normal and high concentration oxygen have been recommended in the literature [16, 17]. Niu et al. showed in a study performed on Sprague Dawley rats who inhaled carbon dioxide gas that the levels of serum troponin I (CTNI), CK, serum potassium (K), and AST are lower afterwards when treated with hyperbaric oxygen therapy compared to other oxygen treatments (p < 0.05). Levels of serum sodium (Na) and Chloride (Cl) were higher in hyperbaric therapy (p < 0.05). There was no significant difference in pH, PO₂, and PCO₂ among all oxygen-therapy groups (p > 0.05); however, there were significantly less pathological changes in the lungs with hyperbaric therapy [17]. On the other hand, high concentrations of oxygen raise venous pO₂ which reduces the solubility of carbon dioxide in the blood. With no changes in the metabolic conditions, this in turn causes pCO₂ in the venous blood to rise. Due to this so-called Haldane effect, an initial increase of pCO₂ in the bloodstream is to be expected when giving oxygen to a hypoxic carbon dioxide intoxicated person. It has also been suggested that due to high concentrations of oxygen, an increase in dead space is to be expected. P_ETCO2 might therefore underestimate PaCO₂. Other studies have found that there is no significant effect between administering normal levels of oxygen or hyperoxic gas [16, 17].

Diagnosing CO₂ intoxication is in the first place based on scene investigation and circumstances surrounding a victim [18]. Blood analysis will show increased carbon dioxide levels but is not always available pre-hospital [15]. Ischemic ECG changes (ST-segment changes and T-wave inversion) have also been described in several cases [19]. Victims might have burn wounds from contact with dry ice [15]. During massive geothermal emission events in Cameroon, cutaneous erythema and bullae have also been associated with coma states caused by exposure to carbon dioxide in the air on an unknown proportion of corpses and 161 (19%) survivors treated in a hospital. Though, it needs to be said that these were not reported in any other carbon dioxide case without contact to other acidic gasses [13].

Post-mortem identification of carbon dioxide intoxication might even be more difficult. External examination of the body is often unremarkable [1, 7]. Although, bruises and hematoma might be present from CPR or from other rescue efforts [10]. Blood analysis for CO₂ content has only a limited diagnostic value, as CO₂ rapidly accumulates after death [18]. Nevertheless, a case study in Japan showed higher levels of CO₂ than those in the blood of deceased healthy persons. The levels found were similar to samples of fire victims, though there was no carbon monoxide (CO) found in this case (something that is usually found in fire victims) [8]. Analysis of lung gasses might also assist in determining the cause of death: an elevated CO₂ content in lung gasses has been described after vacuum degassing of the lungs in an argon atmosphere and quadrupole-mass-spectrometry [10]. Victims might also show passive hyperemia of the internal organs, pleural petechiae, and edema with a moderate congestion of the lungs and the brains [1, 7, 10]. Due to the limited possibilities of proving lethal CO2 intoxications post-mortem, a close communication is needed among all of the involved parties, especially pre-hospital responders [9].

When confronted with patients with carbon dioxide intoxication, the immediate removal of the casualty (and unprotected rescuers) from the toxic environment is needed [15]. Oxygen should be administered, and appropriate supportive care is advisable [15]. Relating to treatment, both normal and high concentration oxygen have been recommended in the literature, without a definite consensus being reached at the moment. Benefits of each approach have been discussed earlier within the topic “CO₂ toxicity in humans” [16, 17].