Clinical Study of Respiration and Circulation at Fluothane Anaesthesia Part Ⅰ Respiration at Fluothane Anaesthesia

1) Fifty-three patients of good risk, aged between 24 and 64 years were utilized for this study. An analysis was made on respiratory-rate, -volume, tidal volume, expiratory CO(2)-content and blood CO(2)-content at F-O anaesthesia which was carried out in various mathodes; with 2% F-O for 25 minutes, or with 2% F-O for 5, 10 and 15 minutes followed by 1% F-O. One-half mg. of atropine was tried in some cases as preoperative medication. 2) In both cases of 2% F-O alone and 2% F-O followed by 1% F-O inhalation, an increased respiratory rate and, in contrast, a decrement of respiratory volume and markedly of tidal volume were observed. 3) Preoperative medication of atropine decreased such tendencies in grade compared with non-atropine group. It seems to be apparent that atropine preoperative medication acts against respiratory inhibition of Fluothane. 4) The changes of respiratory rate, -volume and tidal volume under 2% F-O anaesthesia can be slightly recovered at the switch over to 1% F-O anaesthesia. which is more noticed when atropine was used. The tidal volume, however, can not be recovered above the physiologically minimum level in any case. 5) The CO(2) content in expiratory air was observed to be increased as the anaesthesia was deepened, which was, to some extent, inhibited by atropine. The content in the end tidal air, however, always increased above the physiological level in all cases. 6) Although the blood CO(2) content was also increased by F-O anaesthesia, it was a little over the physiological limite of the variation. 7) Bennett assistor markedly inhibited the CO(2) contents both in expiratory air and in blood

Clinical Study of Respiration and Circulation at Fluothane Anaesthesia Part Ⅲ Fluothane-Oxygen Anaesthesia with EEG and its blood concentration

Technique: An attempt was made to study a correlation of EEG, clinical anaesthetic depth and Fluothane concentration in blood by the Robson's method at Fluothane-Oxygen anaesthesia. Fourty-two adult human cases of both sexes, having no abnormal manifestations on EEG in awake state, were utilized for this analysis. Demerol, scopolamine and pentobarbital calcium were given in each case as a preoperative medication. Two % of F-O inhalation with semiclosed method was introduced for 25 minutes through a tracheal tube which has been inserted under consciousness by means of superior laryngeal nerve and translaryngeal blocking with 2 % xylocaine. 1) No EEG variation was observed in any case of the preoperative medication. 2) During F-O anaesthesia, however, a characteristic EEG patterns were found; increased amplitude and decreased frequency as the anaesthetic depth deepens. But slow waves were not detected until the depth becomes the 3rd plane of the Ⅲ stage or without hypercarbia. 3) The Fluothane concentration in blood appeares to be increased which the anaesthetic depth is deepened. 4) It seems to be concluded that both EEG manifestations and Fluothane concentration in blood maintain a parallel relation with the depth of F-O anesthesia. This is illustrated as follows

Clinical Study of Respiration and Circulation at Fluothane Anaesthesia Part Ⅲ Fluothane-Oxygen Anaesthesia with EEG and its blood concentration

Technique: An attempt was made to study a correlation of EEG, clinical anaesthetic depth and Fluothane concentration in blood by the Robson's method at Fluothane-Oxygen anaesthesia. Fourty-two adult human cases of both sexes, having no abnormal manifestations on EEG in awake state, were utilized for this analysis. Demerol, scopolamine and pentobarbital calcium were given in each case as a preoperative medication. Two % of F-O inhalation with semiclosed method was introduced for 25 minutes through a tracheal tube which has been inserted under consciousness by means of superior laryngeal nerve and translaryngeal blocking with 2 % xylocaine. 1) No EEG variation was observed in any case of the preoperative medication. 2) During F-O anaesthesia, however, a characteristic EEG patterns were found; increased amplitude and decreased frequency as the anaesthetic depth deepens. But slow waves were not detected until the depth becomes the 3rd plane of the Ⅲ stage or without hypercarbia. 3) The Fluothane concentration in blood appeares to be increased which the anaesthetic depth is deepened. 4) It seems to be concluded that both EEG manifestations and Fluothane concentration in blood maintain a parallel relation with the depth of F-O anesthesia. This is illustrated as follows

Clinical Study of Respiration and Circulation at Fluothane Anaesthesia Part Ⅱ Circulation at Fluothane Anaesthesia

1) Eighty four patients aged between 24 and 64 years were utilized for this study with 2% F-O inhalation for 25 minutes or with 2% F-O for 5, 10 and 15minutes followed by 1% F-O. The maximam B. P., pulse rate, and pulse pressure were analysed. Atropine was used in some cases as a preoperative medication. Another group of 15 patients, having been inserted a tracheal tube under consciousness, was checked on cardiac-output, -index, stroke volume, circulatory blood volume and total peripheral resistance both before and 15 minutes after 2% F-O anaesthesia. Bennett assistor was used in some cases. EKG observation was also done. 2) In case of 2% F-O anaesthesia. an immediate decrement of BP was found in value of about 40 mmHg. Atropine seemed to be little effective against the decrement. 3) A recovery of the BP decrement was observed when 2% F-O was replaced by 1% F-O. 4) Although bradycardia was observed during the anaesthesia of both 1% and 2% F-O, atropine could absolutely inhibit it. 5) The decreased pulse pressure at F-O anaesthesia is apt to be furthermore intensified by preoperative medication of atropine. This is one of the criteria against the regular routine preoperative medication of atropine and to suggest that the side-effects of F-O anaesthesia in circulation and respiration should be taken account under the base of controling the F-O concentration. 6) It seems to be apparent that the BP drop by F-O inhalation is mainly due to the central inhibition of vasomotor system with the secondary dilatation of peripheral vessels, in addition to the inhibiting mechanism of cardiac muscle which causes the decrement of cardiac output. 7) EKG obsevations reveal a vagotonic state with nodal rhythm at F-O anaesthesia in most cases. Ischemia of cardiac muscle manifesting flattening or invertion of T-wave can not be observed. The improvement of preoperative EKG would rather be found in a number of cases