Improved hemodynamic performance with a novel chest compression device during treatment of in-hospital cardiac arrest

被引:145
作者
Timerman, S
Cardoso, LF
Ramires, JAF
Halperin, H
机构
[1] Johns Hopkins Med Inst, Dept Med, Div Cardiol, Baltimore, MD 21205 USA
[2] Johns Hopkins Med Inst, Dept Biomed Engn, Div Cardiol, Baltimore, MD 21205 USA
[3] Johns Hopkins Med Inst, Div Radiol, Div Cardiol, Baltimore, MD 21205 USA
[4] Univ Sao Paulo, Sch Med, Inst Heart, InCor, Sao Paulo, Brazil
关键词
cardiopulmonary resuscitation; coronary perfusion pressure; cardiac arrest; chest compression;
D O I
10.1016/j.resuscitation.2004.01.025
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Introduction: The purpose of this pilot clinical study was to determine if a novel chest compression device would improve hemodynamics when compared to manual chest compression during cardiopulmonary resuscitation (CPR) in humans. The device is an automated self-adjusting electromechanical chest compressor based on AutoPulse(TM) technology (Revivant Corporation) that uses a load distributing compression band (A-CPR) to compress the anterior chest. Methods: A total of 31 sequential subjects with in-hospital sudden cardiac arrest were screened with institutional review board approval. All subjects had received prior treatment for cardiac disease and most had co-morbidities. Subjects were included following 10 min of failed standard advanced life support (ALS) protocol. Fluid-filled catheters were advanced into the thoracic aorta and the right atrium and placement was confirmed by pressure waveforms and chest radiograph. The coronary perfusion pressure (CPP) was measured as the difference between the aortic and right atrial pressure during the chest compression's decompressed state. Following 10 min of failed ALS and catheter placement, subjects received alternating manual and A-CPR chest compressions for 90 s each. Chest compressions were administered without ventilation pauses at 100 compressions/min for manual CPR and 60 compressions/min for A-CPR. All subjects were intubated and ventilated by bag-valve at 12 breaths/min between compressions. Epinephrine (adrenaline) (1 mg i.v. bolus) was given at the request of the attending physician at 3-5 min intervals, Usable pressure signals were present in 16 patients (61 +/- 6 years, 5 female), and data are reported from those patients only. A-CPR chest compressions increased peak aortic pressure when compared to manual chest compression (153 +/- 28 mmHg versus 115 +/- 42 mmHg, P < 0.0001, mean +/- S.D.). Similarly, A-CPR increased peak right atrial pressure when compared to manual chest compression (129 +/- 32 mmHg versus 83 +/- 40 mmHg, P < 0.0001). Furthermore, A-CPR increased CPP over manual chest compression (20 +/- 12 mmHg versus 15 +/- 11 mmHg, P < 0.015). Manual chest compressions were of consistent high quality (51 +/- 20 kg) and in all cases met or exceeded American Heart Association guidelines for depth of compression. Conclusion: Previous research has shown that increased CPP is correlated to increased coronary blood flow and increased rates of restored native circulation from sudden cardiac arrest. The A-CPR system using AutoPulse technology demonstrated increased coronary perfusion pressure over manual chest compression during CPR in this terminally ill patient population. (C) 2004 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:273 / 280
页数:8
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