End-Tidal carbon dioxide changes during cardiopulmonary resuscitation after experimental asphyxial cardiac arrest

• Published in: The American journal of emergency medicine 1996-07, Vol.14 (4), p.349-350
• Main Authors: Bhende, Mananda S, Karasic, Denise G, Karasic, Raymond B
• Format: Article
• Language: English
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Asphyxia - complications; asphyxial cardiopulmonary arrest; Biological and medical sciences; capnometry; Carbon Dioxide - metabolism; Cardiopulmonary Resuscitation; Disease Models, Animal; Dogs; Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care; End-tidal CO 2; Heart Arrest - etiology; Heart Arrest - metabolism; Heart Arrest - therapy; Intensive care medicine; Medical sciences; pediatric canine model
• ISSN: 0735-6757; 1532-8171
• DOI: 10.1016/S0735-6757(96)90046-7

A study was undertaken to determine the pattern of end-tidal carbon dioxide ( etco 2) changes during asphyxia-induced cardiac arrest in a pediatric canine model. Eleven intubated, anesthetized, paralyzed dogs (mean age, 4.1 mo; mean weight, 5.5 kg) were used. Asphyxia was induced by clamping the endotracheal tube (ETT) and discontinuing ventilation. Cardiac arrest ensued a few minutes later, after which closed-chest cardiopulmonary resuscitation (CPR) and ventilation were initiated. The etco 2 level was recorded at baseline and every minute during CPR. Mean baseline etco 2 was 31.9 mm Hg. The initial etco 2 immediately after unclamping the ETT (mean, 35 mm Hg) was higher than subsequent values (mean, 12.4 mm Hg; P < .001). There was a sudden increase in etco 2 to a mean of 27.0 mm Hg at or just before return of spontaneous circulation (ROSC) in all 11 cases ( P < .01). During CPR, etco 2 levels were initially high, decreased to low levels, and increased again at ROSC. This pattern, not previously described, is different from that observed in animal and adult cardiac arrest caused by ventricular fibrillation, during which etco 2 decreases to almost zero after the onset of arrest, begins to increase after the onset of effective CPR, and increases to normal levels at ROSC. In this model of asphyxial arrest, continued cardiac output prior to arrest allows continued delivery of CO 2 to the lungs, resulting in higher alveolar CO 2; this, in turn, is reflected as increased etco 2 once ventilation is resumed during CPR. Further study is needed to determine whether the pattern of etco 2 changes can be used prospectively to define the etiology of cardiac arrest.