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心肺复苏期间胸内压力波动促使血液流动:血流动力学数据与数学模型预测结果的比较

Intrathoracic pressure fluctuations move blood during CPR: comparison of hemodynamic data with predictions from a mathematical model.

作者信息

Halperin H R, Tsitlik J E, Beyar R, Chandra N, Guerci A D

机构信息

Peter Belfer Laboratory for Myocardial Research, Department of Medicine, Johns Hopkins Medical Institutions, Baltimore, MD 21205.

出版信息

Ann Biomed Eng. 1987;15(3-4):385-403. doi: 10.1007/BF02584292.

Abstract

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. We developed a mathematical model that predicts that 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, the model predicts that 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. The model was validated for direct cardiac compression by studying the hemodynamics of cyclic cardiac deformation following thoracotomy in four anesthetized, 21-32-kg dogs. As predicted by the model, there was no change in myocardial or cerebral perfusion pressures when the duration of compression 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%. The model was validated for intrathoracic pressure changes by studying the hemodynamics produced by a thoracic vest (vest CPR) in eight dogs. The vest contained a bladder that was inflated and deflated. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was less than 0.8 cm. As predicted by the model and opposite to direct cardiac compression, there was no change in perfusion pressures when the rate was increased from 60 to 150/min at a constant duration of 45% of the cycle. Manual CPR was then studied in eight dogs. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres and behaved as predicted from the model of intrathoracic pressure, not direct cardiac compression. At nearly constant peak sternal force (378-426 N), flow was significantly increased when the duration of compression was increased from short (13%-19% of the cycle) to long (40%-47%), at a rate of 60/min. Flow was unchanged, however, for an increase in rate from 60 to 150/min at constant compression duration. In addition, myocardial and cerebral flow correlated with their respective perfusion pressures.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

心肺复苏(CPR)期间的血流是由胸内压力波动还是直接心脏按压引起的,这一问题仍存在争议。我们开发了一个数学模型,该模型预测,胸内压力波动导致的血流在很宽的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,该模型预测血流应取决于按压速率和力,但超过阈值后,对按压持续时间不敏感。速率和持续时间变化所产生的这些血流动力学差异,构成了确定CPR期间的血流是由胸内压力波动还是由心脏直接按压引起的基础。通过研究4只体重21 - 32千克的麻醉犬开胸后周期性心脏变形的血流动力学,对该模型用于心脏直接按压的情况进行了验证。正如模型所预测的,当按压持续时间从周期的15%增加到45%而速率保持在60次/分钟不变时,心肌和脑灌注压没有变化。然而,当速率从60次/分钟增加到150次/分钟而持续时间保持在45%不变时,灌注压显著增加。通过研究8只犬使用胸部背心(背心式CPR)产生的血流动力学,对该模型用于胸内压力变化的情况进行了验证。该背心包含一个可充气和放气的气囊。背心式CPR在没有直接心脏按压的情况下改变了胸内压力,因为胸骨位移小于0.8厘米。正如模型所预测的且与心脏直接按压相反,当速率从60次/分钟增加到150次/分钟而持续时间保持在周期的45%不变时,灌注压没有变化。然后对8只犬进行了徒手CPR研究。未对胸部进行手术操作。用放射性微球测定心肌和脑血流量,其表现与胸内压力模型预测的一致,而非心脏直接按压模型。在胸骨峰值力几乎恒定(378 - 426牛)的情况下,当按压持续时间从短(周期的13% - 19%)增加到长(40% - 47%)且速率为60次/分钟时,血流量显著增加。然而,当按压持续时间不变而速率从60次/分钟增加到150次/分钟时,血流量没有变化。此外,心肌和脑血流量与其各自的灌注压相关。(摘要截断于400字)

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