Cardiac arrest induced by accidental inhalation of anoxic gases, is the cause always a lack of oxygen?

BACKGROUND

We experienced a case of accidental administration of 100% carbon dioxide (CO2) during anesthesia, which resulted in cardiac arrest. After successful cardio-pulmonary resuscitation the child recovered without brain damage. This outcome was quite different than that of the more commonly reported accidental administration of 100% nituous oxide (N2O), as the latter usually results in death from cerebral damage rather than cardiac arrest. We speculated that the cause of death and/or cardiac arrest may differ between these two anoxic gases.

METHODS

Fourteen dogs were anesthetized and divided into two groups to receive either 100% CO2 or 100% N2O. Blood pressure (BP), heart rate (HR), cardiac output (CO), dp/dt, pulmonary artery pressure (PAP), central venous pressure (CVP) and blood gases (BG) were measured every 30 seconds until cardiac arrest (CA) occurred.

RESULTS

The CO2 group showed a rapid decline in BP, HR, dp/dt, CO, pH, and PaO2 and a rise in PAP, CVP, and PaCO2, with CA occurring at 119 +/- 41 seconds. At the time of CA, the BG values were pH 6.6 +/- 0.09, PaCO2 375 +/- 69, and PaO2 62 +/- 15 mm Hg. The N2O group maintained BP, HR, dp/dt, pH, PaCO2, and experienced a rapid decline in PaO2 as in the CO2 group until 180 seconds, at which time the PaO2 was 12.3 +/- 3 mm Hg. CA occurred at 390 +/- 52 seconds. The values for pH, PaCO2 and PaO2 were 7.5 +/- 0.05, 25 +/- 15 and 4.8 +/- 1 mm Hg, respectively, at the time of CA.

CONCLUSION

One hundred percent CO2-induced cardiac arrest occurred in 119 seconds and was not oxygen-dependent, whereas 100% N2O induced cardiac arrest occurred in 390 seconds and was clearly dependent on hypoxemia.