THE PHYSIOLOGY OF EXTERNAL CARDIAC MASSAGE - HIGH-IMPULSE CARDIOPULMONARY RESUSCITATION
THE PHYSIOLOGY OF EXTERNAL CARDIAC MASSAGE - HIGH-IMPULSE CARDIOPULMONARY RESUSCITATION
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DOI：
10.1161/01.cir.70.1.86
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发表时间：
1984-01-01
期刊：
影响因子：
37.8
通讯作者：
RANKIN, JS
中科院分区：
文献类型：
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作者：
MAIER, GW;TYSON, GS;RANKIN, JS
在完整的长期仪器狗，左心室动力学进行了研究，在心肺复苏（CPR）。电磁流量探头测量心输出量和冠状动脉血流量，超声换能器测量心脏尺寸，微压计测量左心室、右心室、主动脉和胸内压。用吗啡麻醉，插管，通过快速心室起搏使犬颤动。数据是在狗的侧卧位和仰卧位进行手动外部按摩时获得的。压迫力在10-30 mm Hg的峰值胸内压范围内变化，压迫率在60-150/min范围内变化。增加压迫力可增加每搏输出量，直至峰值胸内压为apprx。20 mm Hg，超过该值，每搏输出量保持不变或下降。每搏输出量似乎主要是由手动按压力直接传递到心脏而不是胸内正压引起的，因为心脏或血管压力峰值或这些压力的变化始终是手动按压期间相应胸内压的2-4倍。随着按压速率的增加，每搏输出量保持相对恒定，而总心输出量显著增加：425 ± 0.05。在60分钟时为92 ml/min，643 . ±.在100/min下为130 ml/min，和在975 . ±. 150/min时为219 ml/min（P < 0.05）。在较高的手动按压速率下，左心室尺寸最小程度地减小。在4例接受心肺复苏术的患者中，收缩压和舒张压随着按压速率的加快而升高，与在犬中获得的数据相关性良好。犬实验中的动态冠状动脉血流在压缩过程中下降到零或负值。顺行冠状动脉血流主要发生在非压迫期间，似乎与舒张期主动脉灌注压有关;在150/min的压迫速率下，冠状动脉血流平均为对照的75%。通过中等力度和短暂持续时间的手动胸外按压，使该犬制备中的每搏输出量和冠状动脉血流量最大化。增加按压速率可增加总心输出量，同时维持冠状动脉血流量。直接心脏按压似乎是手动心脏外按摩期间每搏输出量的主要决定因素。
In intact chronically instrumented dogs, left ventricular dynamics were studied during cardiopulmonary resuscitation (CPR). Electromagnetic flow probes measured cardiac output and coronary blood flow, ultrasonic transducers measured cardiac dimensions, and micromanometers measured left ventricular, right ventricular, aortic and intrathoracic pressures. The dogs were anesthetized with morphine, intubated and fibrillated by rapid ventricular pacing. Data were obtained during manual external massage with dogs in the lateral and supine positions. Force of compression was varied from a peak intrathoracic pressure of 10-30 mm Hg, and compression rate was varied from 60-150/min. Increasing force of compression increased stroke volume up to a peak intrathoracic pressure of .apprx. 20 mm Hg, beyond which stroke volume remained constant or declined. Stroke volume appeared to result primarily from direct transmission of manual compression force to the heart rather than from positive intrathoracic pressure because peak cardiac or vascular pressures or the change in these pressures were consistently 2-4 times greater than the corresponding intrathoracic pressures during manual compression. With increasing compression rate, stroke volume remained relatively constant, and total cardiac output increased significantly: 425 .+-. 92 ml/min at 60 min, 643 .+-. 130 ml/min at 100/min, and 975 .+-. 219 ml/min at 150/min (P < 0.05). Left ventricular dimensions decreased minimally at higher manual compression rates. In 4 patients undergoing CPR, systolic and diastolic arterial blood pressure increased with faster compression rates, correlating well with data obtained in the dog. Dynamic coronary blood flow in canine experiments decreased to zero or negative values during compression. Antegrade coronary flow occurred primarily during noncompression periods and seemed to be related to diastolic aortic perfusion pressure; coronary flow at a compression rate of 150/min averaged 75% of control. Stroke volume and coronary blood flow in this canine preparation were maximized with manual chest compression performed with moderate force and brief duration. Increasing rate of compression increased total cardiac output while coronary blood flow was well maintained. Direct cardiac compression appeared to be the major determinant of stroke volume during manual external cardiac massage.