Halothane‐Epinephrine-induced Cardiac Arrhythmias and the Role of Heart Rate
Halothane‐Epinephrine-induced Cardiac Arrhythmias and the Role of Heart Rate
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氟烷-肾上腺素诱发的心律失常和心率的作用
DOI：
10.1097/00000542-197511000-00012
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发表时间：
1975
期刊：
影响因子：
8.8
通讯作者：
P. Dresel
中科院分区：
文献类型：
--
作者：
J. Zink;B. Sasyniuk;P. Dresel
作者先前表明，环丙烷-肾上腺素诱导的二联性心律失常最好用折返机制解释。他们现在已经获得了证据，证明在用0.8%氟烷麻醉的狗中，在输注肾上腺素（0.5 -3 μg/kg/min）时，二联心律失常会折返。临界血压水平和临界心率增加对于在任何给定动物中诱导心律失常都是必要的。在输注阈下剂量肾上腺素时人为升高血压可诱发二联律，突然降低血压可中止心律失常。在二联律发作前，心率加速约40次/min，在阈下输注肾上腺素期间，以类似的加速速率进行心房起搏可诱导二联律。刺激切断的右颈迷走神经的外周端可降低心率，并将二联律转换为窦性心律。心动过缓不是迷走神经效应的唯一机制，因为当通过心房起搏维持心率恒定时，通过更快的迷走神经刺激也可以实现窦性心律的转换。在这些条件下，进一步加速的心率可以恢复二联性心律失常，再次敏感的迷走神经刺激的频率进一步增加，它的结论是，迷走神经的行为上的折返脉冲的传播。这在环丙烷麻醉时表现得最好，因为氟烷更容易发生房室结阻滞。此外，非常短暂的心率增加导致二联律延长，这表明心率变化可能改变氟烷致敏心肌的电生理学，通过折返机制促进二联律心律失常。
The authors previously showed that cyclopropane-epinephrine-induced bigeminal arrhythmias can best be explained by a re-entrant mechanism. They have now obtained evidence for re-entry in bigeminal arrhythmias during infusions of epinephrine (.5–3 μg/kg/min) in dogs anesthetized with .8 per cent halothane. Both a critical level of blood pressure and a critical increase in heart rate were necessary for arrhythmias to be induced in any given animal. Artificial elevation of the blood pressure during infusion of a subthreshold dose of epinephrine could induce bigeminy, and the arrhythmia could be aborted by a sudden reduction of blood pressure. The heart rate accelerated approximately 40 beats/min prior to the onset of bigeminy, and atrial pacing at similarly increased rates during a subthreshold infusion of epinephrine could induce bigeminy. Stimulation of the peripheral end of the cut right cervical vagus reduced heart rate and converted bigeminy to sinus rhythm. Bradycardia was not the sole mechanism of the vagal effect since conversion to sinus rhythm could also be achieved with more rapid stimulation of the vagus when the heart rate was maintained constant by atrial pacing. Under these conditions further acceleration of the heart rate could reinstate a bigeminal arrhythmia that was again sensitive to further increases in the frequency of vagal stimulation, and it is concluded that the vagus acts on the spread of the re-entrant impulse. This is best shown with cyclopropane anesthesia, because AV-nodal block occurs more easily with halothane. In addition, very brief periods of increased heart rate caused prolonged periods of bigeminy, which indicates that changes in heart rate may alter the electrophysiology of the halothane-sensitized myocardium to promote bigeminal arrhythmias by a re-entry mechanism.