DETERMINANTS OF BLOOD-FLOW TO VITAL ORGANS DURING CARDIOPULMONARY-RESUSCITATION IN DOGS
DETERMINANTS OF BLOOD-FLOW TO VITAL ORGANS DURING CARDIOPULMONARY-RESUSCITATION IN DOGS
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DOI：
10.1161/01.cir.73.3.539
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发表时间：
1986-03-01
期刊：
影响因子：
37.8
通讯作者：
WEISFELDT, ML
中科院分区：
文献类型：
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作者：
HALPERIN, HR;TSITLIK, JE;WEISFELDT, ML
心肺复苏（CPR）过程中的血流是由胸内压波动还是直接心脏按压引起的仍存在争议。从建模考虑，由于胸内压力波动引起的血流应该在宽范围内对按压速率不敏感，但取决于施加的力和按压持续时间。然而，如果心脏的直接按压起主要作用，则流量应取决于按压速率和力，但高于阈值，对按压持续时间不敏感。由速率和持续时间的变化产生的血液动力学的这些差异形成了确定CPR期间的血流是由胸内压力波动还是由直接心脏按压引起的基础。在8只麻醉的21 - 32公斤的狗中研究了诱导室颤后的手动CPR。没有对胸部进行手术操作。用放射性微球测定心肌和脑血流量。在几乎恒定的峰值胸骨力（378至426牛顿）下，当压缩持续时间从14 ± 10牛顿增加时，流量显著增加。1%至46 .+-。3%的循环，速率为60/min。然而，在恒定压缩持续时间下，速率从60/min增加到150/min后，流量不变。接下来，将手动CPR的血流动力学与其他8只狗的背心充气同时通气（背心CPR）产生的血流动力学进行了比较。背心CPR改变胸内压而不直接心脏压迫，因为胸骨位移小于0.8 cm。在150/min的速率下，具有相似的持续时间和右心房峰值压力，手动和背心CPR产生相似的流量和灌注压。最后，对开胸后人工心肺复苏与心脏按压的血流动力学进行比较。测量心脏变形，并在速率和持续时间变化期间保持几乎恒定。与伴随手动CPR的变化相反，当持续时间以60/min的恒定速率从15%增加到45%时，灌注压没有变化。然而，当速率以45%的恒定持续时间从60增加到150/min时，灌注压显著增加。因此，在手动胸外按压过程中的重要器官灌注压和流量依赖于ocpressure的持续时间，但不是对大鼠的60或150/min。这些数据是类似的背心CPR，胸内压力是操纵没有胸骨位移，但观察到的直接心脏按压相反。我们的结论是，胸内压力波动在手动心肺复苏期间会产生血流。
Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. From modeling considerations, blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range, but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, however, flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. Manual CPR was studied in eight anesthetized, 21 to 32 kg dogs after induction of ventricular fibrillation. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres. At nearly constant peak sternal force (378 to 426 newtons), flow was significantly increased when the duration of compression was increased from 14 .+-. 1% to 46 .+-. 3% of the cycle at a rate of 60/min. Flow was unchanged, however, after an increase in rate from 60 to 150/min at constant compression duration. The hemodynamics of manual CPR were next compared with those produced by vest inflation with simultaneous ventilation (vest CPR) in eight other dogs. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was less than 0.8 cm. At a rate of 150/min, with similar duration and right atrial peak pressure, manual and vest CPR produced similar flow and perfusion pressures. Finally, the hemodynamics of manual CPR were compared with the hemodynamics of direct cardiac compression after thoracotomy. Cardiac deformation was measured and held nearly constant during changes in rate and duration. As opposed to changes accompanying manual CPR, there was no change in perfusion pressures when duration was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. Thus, vital organ perfusion pressures and flow during manual external chest compression are dependent on the duration of ocmpression, but not on rats of 60 or 150/min. These data are similar to those observed for vest CPR, where intrathoracic pressure is manipulated without sternal displacement, but opposite of those observed for direct cardiac compression. We conclude that intrathoracic pressure fluctuations generate blood flow during manual CPR.