Carbon dioxide narcosis—induced apnea in a rat model of cardiac arrest and resuscitation

• Published in: Resuscitation 1998-09, Vol.38 (3), p.185-191
• Main Authors: Reid, K.H, Patenaude, B, Guo, S.Z, Iyer, V.G
• Format: Article
• Language: English
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Apnea - etiology; Biological and medical sciences; Blood gases; Carbon dioxide; Carbon Dioxide - blood; Cardiac arrest; Cardiopulmonary Resuscitation; Coma - etiology; CPR; Disease Models, Animal; Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care; Evoked Potentials, Auditory, Brain Stem - physiology; Heart Arrest - etiology; Hypercarbia; Intensive care medicine; Male; Medical sciences; Neurologic dysfunction; Oxygen - blood; Oxygen Inhalation Therapy; Pulmonary Gas Exchange; Rats; Rats, Long-Evans; Reaction Time - physiology; Respiration; Respiration, Artificial; Respiratory Insufficiency - therapy; Tidal Volume
• ISSN: 0300-9572; 1873-1570
• DOI: 10.1016/S0300-9572(98)00096-3

In the clinical literature there are reports of patients failing to breathe and becoming comatose when supplied with 100% oxygen for respiratory distress. This effect has been attributed to a loss of respiratory drive. Recent studies have established that this explanation is incorrect, but have left the phenomenon unexplained. We propose that the apnea and coma reported is due to carbon dioxide narcosis. We have reproduced this effect in an animal model and have documented PCO2 values in excess of 250 mmHg during the apneic period. Our results suggest that this level of PCO2 suppresses both brainstem auditory evoked potentials and spontaneous respiration. The high PCO2 is due to inadequate gas exchange, and is easily remedied by provision of adequate ventilation.