Atropine, norepinephrine, and isoproterenol and the cardiac response to experimental lactic acidosis

Abstract

Acute addition lactic acidosis causes marked cardiac slowing, decreased cardiac output, and a progressive rise in the central venous pressure in the dog, suggesting increased vagal activity as well as decreased myocardial function. Bilateral cervical vagotomy and atropine in large dosages were employed to evaluate the role of vagal innervation in producing bradycardia and rhythm changes during acute lactic acidosis. These experimental procedures increased cardiac rate but did not improve cardiac output after the induction of lactic acidosis. Isoproterenol was compared with norepinephrine as a therapeutic agent to improve myocardial function during acidosis. Norepinephrine administration increased arterial pressure by 16 per cent, but did not improve cardiac output or cardiac rate when infused during acidosis. By contrast, isoproterenol caused a 10 per cent fall in arterial pressure, a 93.5 per cent increase in the cardiac output, and a 32 per cent increase in cardiac rate. These experimental findings suggest that increased vagal activity is a cause for the bradycardia and rhythm changes observed during acute lactic acidosis. Isoproterenol was an effective therapeutic agent to improve cardiac output, decrease peripheral resistance, and increase cardiac rate during severe acidosis. The application of these findings to the management of low perfusion states has been discussed.