Atropine-neostigmine mixture

Abstract

To the Editor: The recent study of Naguib and Mohammed 1 leaves me dissatisfied. These investigators studied the doses of atropine required to prevent neostigmine (0.04-0.06 mg.kg -t) from lowering the heart rate below baseline (pre.reversal) in 50 and 95 per cent of patients after antagonism of nondepolarizing neuromuscular blockade with neostigmine-atropine mixtures. They estimated that .the EDso and EDgs values for atropine were approximately 0.035 and 0.055 kg -I respectively. They conclude that appropriate doses of atropine when used with neostigmine should be greater than that used. First, I am not sure that the authors have asked the right question. Is any decrease in heart rate from control really of clinical significance or a valid definition of bradycardia? For example, in group A-I the decrease in mean heart rate from a baseline of 92 to a low of 70 per minute may be statistically significant and real, but is it important? Of far greater interest is the actual number or percentage of patients who manifested heart rates of less than 60 or at least some fixed standard. In addition, in constructing their dose-response relationships the authors have not differentiated between large and small changes in heart rate. A decrease from 90 to 60.min -1 was given the same weight as a decrease from 80 to 70. This is simply not a sensible approach. Second, if commonly used dosages are not appropriate, what practical recommendations do the authors make? Do they suggest that doses of atropine of 0.05 to 0.06 mg. kg -1 should be employed clinically? This is the implied message of the paper and I think a potentially dangerous one. The central nervous system effects of 4 mg of atropine in a 70 kg adult deserve to be mentioned. If the authors really believe that prevention of any decrease in heart rate is a desirable goal and that these doses of atropine are warranted, then the virtues of glycopyrrolate vs atropine must also be discussed.