Spontaneous gasping decreases intracranial pressure and improves cerebral perfusion in a pig model of ventricular fibrillation
Spontaneous gasping decreases intracranial pressure and improves cerebral perfusion in a pig model of ventricular fibrillation
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DOI：
10.1016/j.resuscitation.2005.08.013
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发表时间：
2006-05-01
期刊：
影响因子：
6.5
通讯作者：
Lurie, KG
中科院分区：
文献类型：
--
作者：
Srinivasan, V;Nadkarni, VM;Lurie, KG
引言：在心脏骤停的动物模型和人类的观察性研究中，自发性喘息与生存率增加相关。喘息对脑灌注的潜在有益作用可能是观察到的生存益处的基础，但机制仍不清楚。假设：我们假设，自发喘息在猪模型的心室颤动（VF）降低颅内压（ICP）和增加脑灌注压（CePP），在VF在猪model.Methods：13只雌性农场猪，体重在16和33公斤之间，麻醉与异丙酚和插管，然后有VF诱导8分钟无干预。连续测量胸内压（ITP）、主动脉压（AoP）和ICP。同时记录三个最大喘息期间的CePP和ITP，并通过斯皮尔曼等级相关性将其与喘息相关联。每次喘息都与双相AoP（最初下降，然后上升）和ICP（最初上升，然后fait）形态相关。第一次喘息时间（r（2）= 0.06）、最大喘息时间（r（2）= 0.02）、喘息持续时间（r（2）= 0.11）和喘息频率（r（2）= 0.32）与喘息期间的CePP无显著相关性，而喘息深度与CePP表现出弱但显著的相关性（r（2）= 0.35，p = 0.05）。最大喘息发生在VF发作后202 +/-34 s，导致ICP平均从27.4 +/- 5.8降至20 +/- 6.7 mmHg，p < 0.01沿着CePP从-0.05 +/- 10.9增至11.5 +/- 12.6 mmHg，p <0.05。结论：心脏骤停时的自发性喘息可显著降低颅内压并增加脑灌注压。这些结果可能有助于解释为什么喘息与提高心脏骤停存活率有关。基于对喘息生理学的这种新的理解，我们推测，应该优先研究能够增强喘息对颅内压和脑灌注的生理影响的设备。(c)2005爱思唯尔爱尔兰有限公司保留所有权利。
Introduction: Spontaneous gasping is associated with increased survival in animal models of cardiac arrest and in observational studies of humans. The potential beneficial effect of gasping on cerebral perfusion may underlie the observed survival benefit, but mechanisms remain unknown. Hypothesis: We hypothesized that spontaneous gasping in a pig model of ventricular fibrillation (VF) decreases intracranial pressure (ICP) and increases cerebral perfusion pressure (CePP) during VF in a pig model.Methods: The 13 female farm pigs, weighing between 16 and 33 kg, were anesthetized with propofol and intubated, and then had VF induced for 8 min without intervention. Intrathoracic pressure (ITP), aortic pressure (AoP), and ICP were measured continuously. CePP and ITP were recorded simultaneously during three maximal gasps and correlated with gasping by Spearman rank correlation.Results: Gasping during VF occurred in 13/13 pigs and followed a crescendo-decrescendo pattern. Each gasp was associated with a biphasic AoP (initial fall, then rise) and ICP (initial rise, then fait) morphology. Time to first gasp ( r(2) = 0.06), time to maximal gasp (r(2) = 0.02), duration of gasping (r(2) = 0.11) and frequency of gasping (r(2) = 0.32) did not correlate significantly with CePP during gasping while depth of gasping exhibited a weak but significant correlation with CePP (r(2) = 0.35, p = 0.05). Maximal gasping occurred at 202 +/- 34s from onset of VF and resulted in an average decrease in ICP from 27.4 +/- 5.8 to 20 +/- 6.7 mmHg, p < 0.01 along with an increase in CePP from -0.05 +/- 10.9 to 11.5 +/- 12.6 mmHg, p < 0.05.Conclusions: Spontaneous gasping during cardiac arrest decreased intra-cranial pressure and increased cerebral perfusion pressure significantly. These results may help explain why gasping is associated with improved cardiac arrest survival rates. Based upon this new understanding of the physiology of gasping, we speculate that investigation of devices that can enhance the physiological effects of gasping on intracranial pressure and cerebral perfusion should be prioritized. (c) 2005 Elsevier Ireland Ltd. All rights reserved.