Doses of epinephrine causing arrhythmia during enflurane, methoxyflurane and halothane anaesthesia in dogs

Abstract

THE ASSOCIATION of cardiac arrhythmias with adrenergic drugs and anaesthetic agents has received extensive study. While halothane, cyclopropane and chloroform are among those clearly implicated as "sensitizing" the myocardium, studies of newer inhalation anaesthetic agents have shown relatively less arrhythmogenic potential. However, quantitation of arrhythmogenic action is di~cult because, in most instances, studies have been conducted by invesitgators using different techniques. We have reported recently the comparative effects of the arrhythmic doses of four vasopressors during equivalent levels of isoflurane and halothane anaesthesia in dogs. 1 The results obtained for epinephrine were similar to those described by Joas and Stevens 2 in their evaluation of halothane and isoflurane. In the present study, we have used a similar methodology to evaluate the arrhythmogenicity of two other halogenated ethers, enflurane and methoxyflurane. For comparison, similar studies also were performed on the same animals during halothane anaesthesia. METHODSFifteen experiments were performed on five non-premedicated male mongrel dogs, ranging in weight from 13.4 to 18.0 kg (mean 16.0 kg). Following induction of anaesthesia with the agent under study, each animal's trachea was intubated with a cuffed tracheal tube without the use of muscle relaxants. The methodology employed is shown in Figure 1. Ventilation was maintained with a volume-limited ventilator at approximately 4 per cent end-tidal CO2 concentration as determined by a Godart capnograph. Femoral, arterial and forelimb venous cannulae were placed percutaneously. Phasic and mean arterial pressures were recorded on a direct-writing oseillograph. Each animal was placed supine on a wanning blanket and oesophageal temperatures were measured with a thermistor probe. The ECG (lead II) recorded cardiac rate and rhythm.Each animal was anaesthetized with enflurane, methoxyflurane and halothane on separate occasions, intervals ranging from seven to fourteen days. End-tidal (alveolar) enflurane and halothane concentrations were monitored with a Beckman LB-2 infrared halothane analyzer. The analyzer was calibrated against gas mixtures stored in cylinders. The composition of these mixtures was analyzed by

Cardiovascular Effects of Local Adrenaline Infiltration During Halothane Anaesthesia and Adrenergic Beta‐Receptor Blockade in Man

“…The arrhythmogenic dose of adrenaline during relatively light levels of halothane anaesthesia has been the same in other reports concerning experiments on dogs (JOAS & STEVENS 1971, TUCKER et al 1974, MUNSON & TUCKER 1975, REISNER & LIPPMAN 1975, TUCKER & MUNSON 1975, ZINK et al 1975.…”

Circulatory Effects of Inhalation Anaesthetics in Dogs and Horses

“…Enflurane and methoxyflurane are somewhat intermediary to halothane (lowest) and isoflurane (highest) with regards to catecholamine compatibility (Munson and Tucker, 1975).…”

Dobutamine-induced bradycardia in a dog

“…Unlike xylazine (Muir et al. 1975) and halothane (Munson & Tucker 1975), it increases the arrhythmogenic dose of epinephrine required to induce ventricular arrhythmias in dogs (Lemke et al. 1994).…”

“…Glycopyrrolate is a parasympatholytic drug which is used in dogs to treat bradycardia (Dyson & James-Davies 1990). Unlike xylazine (Muir et al 1975) and halothane (Munson & Tucker 1975), it increases the arrhythmogenic dose of epinephrine required to induce ventricular arrhythmias in dogs (Lemke et al 1994). Because of these two characteristics, it is unlikely that glycopyrrolate would have contributed to the dobutamine-induced bradycardia.…”