RESPIRATORY MUSCLE FATIGUE DURING CARDIOGENIC-SHOCK
RESPIRATORY MUSCLE FATIGUE DURING CARDIOGENIC-SHOCK
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DOI：
10.1152/jappl.1981.51.2.499
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发表时间：
1981-01-01
影响因子：
3.3
通讯作者：
ROUSSOS, C
中科院分区：
文献类型：
--
作者：
AUBIER, M;TRIPPENBACH, T;ROUSSOS, C
在13条自主呼吸的犬上观察了心源性休克（填塞）对呼吸肌功能的影响。将这13只狗与7只人工通气和麻痹的狗进行比较。两组的心输出量均为对照值的25-35%，并保持恒定。所有犬均未出现缺氧。所有自主呼吸的狗平均死亡140只。15 min后处死，7只人工通气犬3 h后全部存活。自主呼吸犬的死亡继发于呼吸衰竭。经颅压在第1小时增加了152 ± 0.01。25%的对照，然后减少了286 ±。相对于动物死亡前的峰值，下降了18%。呼吸系统的机械性能未发生重大变化。尽管每次呼吸时横膈膜和膈神经的综合电活动幅度显著增加，但经颅压仍会降低。心源性休克的复苏失败是由于呼吸肌收缩过程受损所致。人工通气可避免呼吸衰竭和患者存活，这可能具有重要的治疗意义。
The effect of cardiogenic shock (tamponade) on respiratory muscles performance was studied in 13 dogs breathing spontaneously. These 13 dogs were compared to 7 dogs artificially ventilated and paralyzed. Cardiac output amounted in both groups to 25-35% of the control value and was maintained constant. None of the dogs were hypoxic. All the spontaneously breathing dogs died on the average 140 .+-. 15 min after the onset of cardiogenic shock; the 7 dogs artificially ventilated were all alive after 3 h and then killed. Death in the spontaneously breathing dogs was secondary to respiratory failure. Transdiaphragmatic pressure increased during the 1st h by 152 .+-. 25% of control and then decreased by 286 .+-. 18% in relation to the peak value before the death of the animals. No major changes in the mechanical properties of the respiratory system occurred. The decrease in transdiaphragmatic pressure occurred despite a marked increase per breath in the amplitude of the integrated electrical activity of the diaphragm and of the phrenic nerve. The ventilatory failure of cardiogenic shock is due to an impairment of the contractile process of the respiratory muscles. Artificial ventilation avoids respiratory failure and prolongs survival, which may bear important therapeutic implications.