The effects of toxic concentrations of theophylline on oxygen consumption, ventricular work, acid base balance, and plasma catecholamine levels in the dog.

Theophylline poisoning, characterized in part by tachyarrhythmias, hypokalemia, and a metabolic acidosis, is similar to that expected from excessive beta-adrenergic activity. Using a previously described canine model of theophylline poisoning, invasive cardiovascular parameters were determined along with oxygen consumption (VO2), arterial pH, base deficit, and plasma epinephrine (EPI) and norepinephrine (NEPI) concentrations in four control animals (Group 1) and in four animals receiving 140 mg/kg aminophylline intravenously (Group 2). Group 2 animals developed a significant rise in VO2 as compared to controls (P less than .01). Although left ventricular stroke work index was less in Group 2 animals (P less than .01), the sum of the total amount of ventricular work performed by both ventricles per minute did not differ between the two groups (P greater than .15). There was a marked increase in circulating levels of EPI (P less than .01) and NEPI (P less than .01) in Group 2 animals, along with the development of a metabolic acidosis. Catecholamines, which have been shown to produce tachyarrhythmias, increased VO2, hypokalemia, and a metabolic acidosis, may play an important role in the cardiovascular and metabolic effects seen in theophylline poisoning.