Cardiovascular responses of the dog to acute smoke toxicity.
Cardiovascular function and metabolism were investigated during and after an acute bout of smoke inhalation in dogs anesthetized with morphine-chloralose. Smoke was generated from burning charcoal briquets layered with hardwood sawdust. By the end of 8 min of smoke inhalation significant increases occurred in left and right ventricular dP/dt, heart rate, and respiratory rate while aortic blood pressure underwent little or no change. These hemodynamic changes were paralleled by marked increases in carboxyhemoglobin, lactate, plasma epinephrine, and norepinephrine. Arterial blood gases showed significant decreases in PO2 and pH accompanied by a rise in PCO2. The presence of hypoxic hypoxia and hypercapnia was reversed during the postinhalation period, while catecholamines, carboxyhemoglobin, and lactate remained significantly above control. The ECG recorded throughout the experiment generally showed ventricular premature beats, atrioventricular conduction abnormalities, and increases in T wave amplitude. The above data led to the conclusion that acute smoke toxicity causes cardiac and metabolic alterations resulting from widespread stimulation of the sympathetic nervous system.
D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D002263:Carboxyhemoglobin; D002319:Cardiovascular System / Q000503:physiopathology*; D004285:Dogs; D004837:Epinephrine / Q000097:blood; D005260:Female; D006439:Hemodynamics; D007773:Lactates / Q000097:blood; D008297:Male; D009638:Norepinephrine / Q000097:blood; D010100:Oxygen / Q000097:blood; D012119:Respiration; D012906:Smoke / Q000009:adverse effects*
D007773:Lactates; D012906:Smoke; D002245:Carbon Dioxide; D002263:Carboxyhemoglobin; D010100:Oxygen; D009638:Norepinephrine; D004837:Epinephrine