Conduction defects in the aging heart.
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Biomedical subjects
Publications and source records attributed to D B Rao.
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The effects on neuromuscular (NM) function of combinations of relaxants (d-tubocurarine, pancuronium, and succinylcholine) and local anesthetics (cocaine, procaine, lidocaine, etidocaine, and a quaternized derivative of procaine, procaine methobromide) were investigated using the rat's phrenic nerve--hemidiaphragm preparation. Combinations of ineffective concentrations of NM blocking agents with ineffective concentrations of local anesthetics caused a greater than 90% NM block. Preliminary administration of ineffective concentrations of local anesthetics significantly ( p less than 0.001) decreased the ED50 of NM blocking agents. The administration of ineffective concentrations of NM blocking agents caused a similar decrease of the ED50 of local anesthetics. Concentrations of d-tubocurarine and pancuronium which alone produced partial NM block had additive effects. These findings suggest that the interaction of NM blocking agents and local anesthetics consists of true potentiation caused by the different sites of action of the two types of compounds at the NM junction. The degree of potentiation may be enough to cause clinically significant NM block in patients who at the same time receive high enough doses of both agents. In vitro the NM block caused by the combinations of local anesthetics and NM blocking agents can be reversed by 4-aminopyridine.
Induction of anesthesia for aortocoronary bypass surgery was accomplished by the administration of droperidol, morphine, oxygen and nitrous oxide-oxygen in 20 patients. They ranged from 40 to 69 years of age. Premedication consisted of diphenhydramine and morphine. Cardiovascular stability was the most important aspect of the technique. Heart rate changes were insignificant. Cardiac index increased substantially after droperiodol and remained unchanged after morphine. It stayed around control levels for the rest of the induction. A substantial decrease was observed while using mechanical ventilation. Mean arterial pressure dropped significantly after droperidol and again after morphine, then rose about 17% after oxygen to near control levels, where it stayed thereafter. Peripheral vascular resistance dropped substantially after droperidol. A significant increase occurred after oxygen, reaching almost control levels at this point. Mechanical ventilation caused a significant increase, similar to the decrease in the cardiac index. Decreased oxygen availability was compensated for by decreased oxygen consumption. Induction of neurolept anesthesia in the manner described appears to be void of the undesirable effects of either large doses of morphine, or nitrous oxide-oxygen following such morphine doses. Amnesia was complete in every patient.