Effects of carbon monoxide inhalation on ventricular fibrillation.
Since, in a previous study, inhalation of carbon monoxide resulted in demonstrable electrocardiographic effects on the myocardium, it was of interest to determine the effects of reduced hemoglobin oxygen content following carbon monoxide inhalation on the vulnerability of the heart to fibrillation. Normal monkeys and monkeys subjected to myocardial infarction were exposed to 100 ppm (115 mg/cu m) carbon monoxide for six hours, and the vulnerability of the heart to induced fibrillation was evaluated. The mean carboxyhemoglobin (COHb) concentration attained was 9.3%. The voltage required to induce fibrillation was highest for normal, air-breathing animals and lowest for infarcted animals inhaling carbon monoxide. Infarction alone and carbon monoxide alone each required significantly less voltage for fibrillation, and when the two were combined, the effects were additive.
D000136:Acid-Base Equilibrium; D000818:Animals; D001273:Atmosphere Exposure Chambers; D001831:Body Temperature; D002245:Carbon Dioxide / Q000097:blood; D002248:Carbon Monoxide / Q000494:pharmacology; D002249:Carbon Monoxide Poisoning / Q000150:complications*; D002263:Carboxyhemoglobin / Q000032:analysis; D000882:Haplorhini; D006352:Heart Ventricles / Q000187:drug effects; D008252:Macaca fascicularis; D009203:Myocardial Infarction; D009206:Myocardium / Q000473:pathology; D010100:Oxygen / Q000097:blood; D014693:Ventricular Fibrillation / Q000139:chemically induced*
D002245:Carbon Dioxide; D002248:Carbon Monoxide; D002263:Carboxyhemoglobin; D010100:Oxygen