Anesthetic, Circulatory and Respiratory Effects of Fluothane

Burnap, Thomas K.; Galla, Stephen J.; Vandam, Leroy D.

doi:10.1097/00000542-195805000-00001

Cited by 80 publications

(20 citation statements)

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“…Black, Clarke, Howard & McCullough (1969), on the other hand, recorded extraventricular beats in only two of eleven cats anaesthetized with halothane. Recordings in man indicate that the incidence of arrhythmias during halothane anaesthesia is of the order of 15 to 20% (Burnap et al, 1958;Hellewell & Potts, 1965;Johnstone, 1966a, b;Stephen et al, 1957;Wyant et al, 1958). It should be noted, however, that two groups of workers state specifically that abnormalities of cardiac rhythm occur in man only in the presence of hypercarbia (Black, Linde, Dripps & Price, 1959;Payne & Senfield, 1964).…”

Section: Discussionmentioning

confidence: 99%

“…Arrhythmias have also been recorded during halothane anaesthesia in man (Burnap, Galla & Vandam, 1958;Hellewell & Potts, 1965;Johnstone, 1966a, b;Stephen, Grosskreutz, Lawrence, Fabian, Bourgeois-Gavardin & Coughlin, 1957;Wyant, Merriman, Kilduff & Thomas, 1958), although the incidence appears to be less frequent than in the cat. Under halothane anaesthesia, irregularities of cardiac rhythm were not recorded in the dog by Raventos (1956), but in the horse arrhythmias were reported by Vasko (1962) and Eberly, Gillespie, Tyler & Fowler (1968).…”

Section: Introductionmentioning

confidence: 99%

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Influence of halothane and catecholamines on heart rate and rhythm in the horse

Lees

Tavernor

1970

British J Pharmacology

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Summary1. Ventricular ectopic beats were recorded in eight of thirteen conscious horses following the intravenous administration of adrenaline in doses of 3 t4g/kg. Following pre-treatment with either atropine sulphate (0-1 mg/kg) or propranolol hydrochloride (0O1 mg/kg), the same dose level of adrenaline failed to produce ventricular ectopic beats. 2. Halothane anaesthesia sensitized the equine heart to the arrhythmogenic actions of adrenaline; the incidence and duration of ventricular arrhythmias being greater than in conscious animals. In comparison with the findings in conscious horses, ether anaesthesia appeared to protect the heart against adrenaline-induced arrhythmias.3. From a comparison of the arrhythmogenic, chronotropic and pressor actions of adrenaline, noradrenaline and isoprenaline during halothane anaesthesia. it was concluded that sensitization to the arrhythmogenic actions of catecholamines resulted primarily from the action of halothane on the ventricle. The results also indicated that the pressor responses to catecholamines during halothane anaesthesia probably played some part in the genesis of arrhythmias. 4. No " spontaneous " ventricular arrhythmias were recorded in twenty-four horses anaesthetized with halothane or in sixteen animals under ether anaesthesia. 5. The available evidence indicates that a moderate to fairly severe degree of hypercapnia produced little increase in sympathetic control of the myocardium during halothane anaesthesia; the absence of irregularities in ventricular rhythm during halothane anaesthesia were attributed to this factor.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Influence of halothane and catecholamines on heart rate and rhythm in the horse

Lees

Tavernor

1970

British J Pharmacology

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“…percentage retention at the one-week and three-week post-exposure periods, but the figures do not differ significantly from those in Table I. al., 1958;Burnap et al, 1958;Carson et al, 1959;Griffiths and Ozguc, 1964;Joseph, 1964;Keeri-SzAt6, 1965), Retention (± S.D.) after in dogs (Brindle et al, 1957), in sheep (Hull and Reilly, 1968), res and in calves (Middleton et al, 1966 (Combes and Stakelum, 1962) to support the view that the 5 ±3 6±3 removal of B.S.P.…”

Section: Isolated Liver Perfusionsmentioning

confidence: 87%

Multiple Halothane Exposure and Hepatic Bromsulphthalein Clearance

Biebuyck

Saunders

Harrison

et al. 1971

Survey of Anesthesiology

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“…Since 1958 (Burnap et al 1958; Virtue and Payne 1958), however, evidence has been accumulating that the hepatic damage may be caused by halothane exposure (Barton 1959;Peters et al 1969;Mushin et al 1971;Trowell et al 1975;Wright et al 1975). The criteria for the diagnosis of halothane hepatotoxicity described in those reports are as follows: absence of other known causes of hepatitis; postoperative fever without any obvious cause (Hughes and Powell 1970); jaundice of the hepatocellular type occurring within two weeks of halothane exposure (Inman and Muslim 1974); eosinophilia and infiltration of plasma cells in the liver (Klion et al 1969).…”

Section: Saito K and Kumagai K Postoperative Hepatitis Induced Bymentioning

confidence: 99%