7匹绞痛马麻醉期间的低氧血症

C.M. Trim , P.Y. Wan
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引用次数: 21

摘要

回顾了1987年6月至1989年5月间对马进行肠绞痛麻醉的麻醉记录。在157次手术中进行了pH值和血气分析,这些手术允许马恢复。其中7匹马在麻醉期间测得PaO2为8.0 kPa或更低。这些马的品种、年龄和性别各不相同。4匹马用噻嗪、愈创甘油醚和氯胺酮麻醉,3匹马用噻嗪、愈创甘油醚和硫巴比妥麻醉。麻醉使用吸入麻醉剂和氧气维持:五匹马使用异氟烷,一匹马使用氟烷,最初使用氟烷,后来使用异氟烷。麻醉时收缩压在80 ~ 150mmhg之间,舒张压在60 ~ 128mmhg之间,心率在28 ~ 44次/分之间。麻醉开始时进行控制通气。3匹马的PaCO2超过6.7 kPa,但随后通过调整呼吸机降低。在麻醉早期测得PaO2为8.0 kPa或更低,除一例例外,并在麻醉期间持续存在。在麻醉恢复期间,马的吸入空气中补充了氧气,同时测量了三匹马的血气,结果显示PaO2没有增加。从麻醉中恢复是平静的。手术问题主要涉及五匹马的大肠和两匹马的小肠。六匹马活着出院;当天晚些时候,一匹马被再次麻醉,没有恢复意识就被杀死了。我们的结论是,麻醉前评估中记录的客观值都不能用于预测术中低氧血症的并发症。我们观察到,一旦出现低氧血症,它在麻醉期间持续存在,甚至进入马侧卧和恢复意识的恢复期。我们认为,麻醉剂和低温引起的代谢改变,加上适当的外周灌注,导致6匹马没有出现不良后果。低氧血症对第七匹马病情恶化的影响是推测性的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hypoxaemia during anaesthesia in seven horses with colic

Anaesthetic records of horses with colic anaesthetised between June 1987 and May 1989 were reviewed. pH and blood gas analyses were performed during 157 operations from which the horses were allowed to recover. A PaO2 of 8.0 kPa or less was measured during anaesthesia in seven of these horses. The horses were of different breeds, ages and sexes. Anaesthesia was induced with xylazine, guaifenesin and ketamine in four horses and with xylazine, guaifenesin and thiobarbiturate in three horses. Anaesthesia was maintained with inhalation anaesthetic agent and oxygen: isoflurane in five horses, halothane in one horse, and initially halothane but later isoflurane in one horse. Systolic arterial pressures during anaesthesia ranged from 80 to 150 mmHg, diastolic arterial pressures were between 60 and 128 mmHg, and heart rates were between 28 and 44 beats /min. Controlled ventilation was initiated at the start of anaesthesia. PaCO2 exceeded 6.7 kPa in three horses but was subsequently decreased by adjustment of the ventilator. PaO2 of 8.0 kPa or less was measured during early anaesthesia, with one exception, and persisted for the duration of anaesthesia. The horses' inspired air was supplemented with oxygen during recovery from anaesthesia, at which time measurement of blood gases in three horses revealed no increase in PaO2. Recovery from anaesthesia was uneventful. The surgical problems involved primarily the large intestine in five horses and the small intestine in two horses. Six horses were discharged from the hospital alive; one horse was reanaesthetised later the same day and destroyed without regaining consciousness. We concluded that none of the objective values recorded during the pre-anaesthetic evaluation could have been used to predict the complication of intraoperative hypoxaemia. We observed that once hypoxaemia developed it persisted for the duration of anaesthesia and even into the recovery period when the horses were in lateral recumbency and regaining consciousness. We assume that the altered metabolism from anaesthetic agents and hypothermia combined with adequate peripheral perfusion contributed to the lack of adverse consequences in six of the horses. The contribution of hypoxaemia to the deteriorating condition of the seventh horse is speculative.

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