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大量的研究表明,急性呼吸衰竭时多伴有心血管功能的损害,但有关急性呼吸衰竭对于左室心肌收缩性的影响所知甚少。本文对开胸麻醉犬在低通气引起呼吸衰竭时,左室心肌收缩性的变化进行了观测和分析。结果表明,在实验组(n=9)低通气呼吸(通气量小于160ml/min/kg,PaO_2小于60mmHg)时,心率(HR)、主动脉平均压(MOP)、左室收缩峰压(LV-SP)、左室内压最大上升速率(dP/dt_(max))、节段心肌发展张力(DT)及其最大发展速率(dT/dt_(max))均显著降低,心肌开始收缩至dp/dt_(max)的时间(t-dp/dt_(max))和至dT/dt_(max)的时间(t-dT/dt_(max))则显著增加,与低通气呼吸前比较均有统计学差异。而在对照组(n=5)保持正常通气(通气量大于450ml/min/kg,PaO_2大于70mmHg),观察45min,未见上述指标有明显改变。本研究表明,急性呼吸衰竭时左室心肌收缩性严重受损。
Numerous studies have shown that acute respiratory failure is often associated with impairment of cardiovascular function, but little is known about the effects of acute respiratory failure on left ventricular contractility. In this paper, the changes of left ventricular contractility after thoracotomy anesthesia dogs with respiratory failure caused by hypoventilation were observed and analyzed. The results showed that heart rate (HR), average aortic pressure (MOP), peak systolic pressure of left ventricle (LV) and left ventricular systolic pressure -SP, dP / dt max, DT and its maximum rate of dT / dt max decreased significantly, and myocardial contractility began to decrease to dp / dt max, dt_max, t-dp / dt_max, and time to dT / dt_max (t-dT / dt max) were significantly increased compared with those before ventilation difference. In the control group (n = 5) maintained normal ventilation (ventilation greater than 450ml / min / kg, PaO_2 greater than 70mmHg), observed 45min, no significant changes in the above indicators. This study shows that left ventricular contractility is severely impaired in acute respiratory failure.