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四肢瘫痪患者反射性心脏骤停的机制。

Mechanisms of reflex cardiac arrest in tetraplegic patients.

作者信息

Frankel H L, Mathias C J, Spalding J M

出版信息

Lancet. 1975 Dec 13;2(7946):1183-5. doi: 10.1016/s0140-6736(75)92662-8.

Abstract

Four patients with physiologically complete high cervical spinal-cord lesions, sustained within the previous 6 weeks, were observed. All needed intermittent positive-pressure ventilation. In the stage of spinal shock, stimuli to the trachea induced bradycardia, and in two patients cardiac arrest resulted. The bradycardia occurred when the patients were hypoxic, and seemed to be due to a vaso-vagal reflex. Normally this reflex is opposed by sympathetic activity, and during hypoxia by increased pulmonary (inflation) vagal reflex activity due to increased breathing. In these patients, however, compensatory sympathetic activity was prevented by the cervical cord lesion, and increased pulmonary vagal reflex activity by the fact that the breathing was artificial and therefore did not increase with hypoxia. Treatment in emergency includes the administration of atropine. Adequate oxygenation and, if this cannot be achieved, maintenance atropin should prevent the bradycardia and cardiac arrest associated with stimulation of the trachea in artificially ventilated tetraplegic patients.

摘要

观察了4例在过去6周内发生生理性完全性高位颈脊髓损伤的患者。所有患者均需要间歇性正压通气。在脊髓休克阶段,刺激气管会诱发心动过缓,有2例患者发生心脏骤停。心动过缓发生在患者缺氧时,似乎是由于血管迷走反射。正常情况下,这种反射会受到交感神经活动的对抗,而在缺氧时,由于呼吸增加,肺(充气)迷走反射活动增强。然而,在这些患者中,颈髓损伤阻止了代偿性交感神经活动,并且由于呼吸是人工的,因此不会随着缺氧而增加,从而导致肺迷走反射活动增强。紧急治疗包括使用阿托品。充分的氧合,如果无法实现,则持续使用阿托品应可预防人工通气的四肢瘫痪患者因刺激气管而出现的心动过缓和心脏骤停。

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