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Resuscitation 85 (2014) 683–688

Contents lists available at ScienceDirect

Resuscitation

j ourna l h o me pa g e : www.elsev ier .com/ locate / resusc i ta t ion

xperimental paper

iniaturized mechanical chest compressor improves calculatederebral perfusion pressure without compromising intracranialressure during cardiopulmonary resuscitation in a porcine model ofardiac arrest�

iefeng Xua,d, Xianwen Hua, Zhengfei Yanga, Xiaobo Wua, Joe Biseraa,b,hijie Suna,b, Wanchun Tanga,b,c,∗

Weil Institute of Critical Care Medicine, Rancho Mirage, CA, United StatesKeck School of Medicine of the University of Southern California, Los Angeles, CA, United StatesDepartment of Emergency Medicine, School of Medicine of the University of California, San Diego, CA, United StatesDepartment of Emergency Medicine, Yuyao People’s Hospital, Medical School of Ningbo University, Ningbo, China

r t i c l e i n f o

rticle history:eceived 18 July 2013eceived in revised form 6 January 2014ccepted 10 January 2014

eywords:ardiopulmonary resuscitationardiac arrestemodynamicserebral perfusion pressure

ntracranial pressureiniaturized chest compressor

a b s t r a c t

Objective: One of the major goals of cardiopulmonary resuscitation (CPR) is to provide adequate oxy-gen delivery to the brain for minimizing cerebral injury resulted from cardiac arrest. The optimal chestcompression during CPR should effectively improve brain perfusion without compromising intracranialpressure (ICP). Our previous study has demonstrated that the miniaturized mechanical chest compressorimproved hemodynamic efficacy and the success of CPR. In the present study, we investigated the effectsof the miniaturized chest compressor (MCC) on calculated cerebral perfusion pressure (CerPP) and ICP.Methods: Ventricular fibrillation was electrically induced and untreated for 7 min in 13 male domesticpigs weighing 39 ± 3 kg. The animals were randomized to receive mechanical chest compression with theMCC (n = 7), or the Thumper device (n = 6). CPR was performed for 5 min before defibrillation attempt by asingle 150 J shock. At 2.5 min of CPR, the epinephrine at a dose of 20 �g/kg was administered. Additionalepinephrine was administered at an interval of 3 min thereafter. If resuscitation was not successful, CPRwas resumed for an additional 2 min prior to the next defibrillation until successful resuscitation or fora total of 15 min. Post-resuscitated animals were observed for 2 h.Results: Significantly greater intrathoracic positive and negative pressures during compression anddecompression phases of CPR were observed with the MCC when compared with the Thumper device.The MCC produced significantly greater coronary perfusion pressure and end-tidal carbon dioxide. Therewere no statistically significant differences in systolic and mean ICP between the two groups; however,both of the measurements were slightly greater in the MCC treated animals. Interestingly, the diastolicICP was significantly lower in the MCC group, which was closely related to the significantly lower nega-

tive intrathoracic pressure in the animals that received the MCC. Most important, systolic, diastolic andmean calculated CerPP were all significantly greater in the animals receiving the MCC.Conclusions: In the present study, mechanical chest compression with the MCC significantly improvedcalculated CerPP but did not compromise ICP during CPR. It may provide a safe and effective chestcompression during CPR.

Protocol number: P1205.

© 2014 Elsevier Ireland Ltd. All rights reserved.

� A Spanish translated version of the abstract of this article appears as Appendix in the

∗ Corresponding author at: Weil Institute of Critical Care Medicine, 35100 Bob Hope DrE-mail addresses: Jeff.xu11@gmail.com (J. Xu), xianwenhu@yahoo.com.cn (X. Hu), Yan

bisera@weiliccm.org (J. Bisera), Shijie.sun@aol.com (S. Sun), Wanchun.tang@me.com (W

300-9572/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved.ttp://dx.doi.org/10.1016/j.resuscitation.2014.01.014

final online version at http://dx.doi.org/10.1016/j.resuscitation.2014.01.014.ive, Rancho Mirage, CA 92270, United States.gzhengfei@vip.163.com (Z. Yang), Mike wu@weiliccm.org (X. Wu),. Tang).

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. Introduction

The primary goal of cardiopulmonary resuscitation (CPR) is tostablish the critical levels of blood flow to the heart and brain untilpontaneous circulation is restored. High-quality chest compres-ion has been recognized as the key determinant for the success ofesuscitation. The latest guidelines emphasize that chest compres-ion should be performed with adequate rate and depth, completehest recoil and minimized pauses.1 Conventional manual CPR isimple, quick, inexpensive and always available; however, evenhest compression provided by trained or experienced rescuersften fails to meet the requirements of guidelines.2,3 In the spe-ific clinical setting such as transferring the patients or vehicularransportation, the quality of manual chest compression is difficulto maintain.4

Mechanical chest compression delivers more consistent andeliable chest compression, eliminates the elements of rescueratigue and compression interruption and could potentially over-ome the limitations of manual chest compression. Recent clinicaltudies have demonstrated that the mechanical devices were ben-ficial to provide continuous chest compression with minimizingo-chest compression intervals during ambulance transportationnd interventional coronary catheterization.5,6

The cerebral blood flow is closely related to cerebral perfusionressure (CerPP), which is defined as the difference between meanortic pressure (MAP) and intracranial pressure (ICP). During theompression phase of CPR, increased intrathoracic pressure is usu-lly accompanied with both increases in MAP and ICP. The increasesn intrathoracic pressure may cause a greater increase in ICP than

AP which result in a decrease in CerPP.7 In the present study,e investigated the effects of a recently developed miniaturizedechanical chest compressor (MCC) on calculated CerPP and ICP

n a porcine model of cardiac arrest (CA). We hypothesized thatechanical chest compression with the MCC would improve cal-

ulated CerPP but would not compromise ICP during CPR.

. Materials and methods

All animals received humane care in compliance with the “Prin-iples of Laboratory Animal Care” formulated by the Nationalociety for Medical Research and the Guide for the Care and Usef Laboratory Animals prepared by the Institute of Laboratory Ani-al Resources and published by the National Institutes of Health

8th edition. Washington, DC, National Academies Press, 2011). Therotocol was approved by the Institutional Animal Care and Useommittee of the Weil Institute of Critical Care Medicine.

.1. Animal preparation

Thirteen male domestic pigs weighing 39 ± 3 kg were fastedvernight with the exception of free access to water. Anesthesiaas initiated by intramuscular injection of ketamine (20 mg/kg)

nd completed by an ear vein injection of sodium pentobarbital30 mg/kg). An additional dose of sodium pentobarbital (8 mg/kg)as injected at hourly intervals to maintain anesthesia. A cuffed

ndotracheal tube was advanced into the trachea. The animalsere mechanically ventilated with a volume controlled ventila-

or (Model MA-1, Puritan Bennett Inc., Carlsbad, CA) with a tidalolume of 15 ml/kg, peak flow of 40 l/min and FiO2 of 0.21. End-idal carbon dioxide (ETCO2) was continuously monitored with

n infrared capnometer (Model NPB-70, Nellcor Puritan Bennettnc., Pleasanton, CA). Respiratory frequency was adjusted to main-ain ETCO2 between 35 and 40 mm Hg. The conventional lead IIlectrocardiogram was continuously monitored by applying three

85 (2014) 683–688

adhesive electrodes to the shaved skin of the right upper and leftupper-and-lower limbs.

For the measurement of ICP, a burr hole of 3 mm in diameterwas drilled in the midst between the left eyebrow and the posteriorbony prominence. A 5 F transducer-tipped Millar catheter (ModelSPC-450S, Millar Instruments Inc., Houston, TX) was inserted 2 cminto the parietal lobe and then reflected ICP continuously. Thecatheter was firmly fixed with bolts and sutures around the skull.For the measurement of aortic pressure and the collection of bloodsamples, a fluid-filled 8 F catheter (Model 6523, USCI, C.R. Bard Inc.,Salt Lake City, UT) was advanced from the right femoral artery intothe thoracic aorta. For the measurements of right atrial pressureand core (blood) temperature, a 7 F pentalumen, thermodilution-tipped catheter (Abbott Critical Care # 41216, Chicago, IL) wasadvanced from the right femoral vein into the right atrium. Bothcatheters were flushed intermittently with saline containing 5 IUbovine heparin per ml. For inducing ventricular fibrillation (VF), a5 F pacing catheter (EP Technologies Inc., Mountain View, CA) wasadvanced from the right subclavian vein into the right ventricle.For the measurement of intrathoracic pressure, another 5 F Millarcatheter was advanced from the incisor teeth into the esophagus fora distance of 35 cm. The position of all catheters was confirmed bycharacteristic pressure morphology and with fluoroscopy. In addi-tion, the depth of chest compression during CPR was measured by alinear potentiometer. The piston of the compressor was positionedin the midline at the level of the fifth interspace. Blood tempera-ture was maintained at 37.5 ± 0.5 ◦C with the aid of a cooling/warmblanket throughout the entire experiment.

2.2. Experimental procedures

Fifteen minutes prior to inducing VF, baseline measurementswere obtained. The animals were randomized by the Sealed Enve-lope Method to receive mechanical chest compression with theMCC (Resuscitation International Inc., Scottsdale, AZ) (n = 7) or theThumper device (Model 1004, Michigan Instruments Inc., GrandRapids, MI) (n = 6). VF was induced by 1 mA alternating currentthrough the 5 F pacing catheter, delivered to the right ventricu-lar endocardium. Mechanical ventilation was discontinued afteronset of VF. Prior to initiating the resuscitation protocol, the pacingcatheter was withdrawn to avoid heart injury during chest com-pression. After 7 min of untreated VF, CPR was started. Both theMCC and Thumper devices were programmed to provide an equalcompression-relaxation interval of 50% duty cycle and the samecompression rate of 100 compressions per minute. The initial com-pression depth of the MCC and Thumper devices was adjusted toachieve a threshold coronary perfusion pressure (CorPP) of above12 mm Hg in 1 min. Coincident with the start of precordial compres-sion, the animals were mechanically ventilated with a tidal volumeof 15 ml/kg, FiO2 of 1.0 and a rate of 10 breaths per minute. After2.5 min of CPR, the first bolus of epinephrine at a dose of 20 �g/kgwas administered. After 5 min of CPR, defibrillation was attemptedwith a single 150-J biphasic waveform electrical shock deliveredbetween the conventional right infraclavicular electrode and theapical electrode with a Heartstart XL defibrillator (Philips MedicalSystem Inc., Andover, MA). If an organized rhythm with a MAP ofabove 50 mm Hg persisted for an interval of 5 min or more, the ani-mal was regarded as return of spontaneous circulation (ROSC). Withfailure to achieve ROSC, chest compression and ventilation wereimmediately resumed for 2 min prior to another defibrillation. Theprotocol was repeated until successful resuscitation or for a totalof 15 min. Additional doses of epinephrine were administered at

an interval of 3 min after the first bolus injection. After success-ful resuscitation, the animals were observed for 2 h. If a recurrentVF occurred after ROSC, a 150-J electrical shock was attempted.Mechanical ventilation was continued with FiO2 of 1.0 for 30 min,

J. Xu et al. / Resuscitation 85 (2014) 683–688 685

Table 1Baseline characteristics.

MCC Thumper p

Body weight (kg) 38.1 ± 1.9 39.2 ± 3.5 0.49Heart rate (beats min−1) 114 ± 8 118 ± 9 0.47MAP (mm Hg) 107 ± 6 109 ± 6 0.49End-tidal CO2 (mm Hg) 39.9 ± 1.7 39.7 ± 0.5 0.79SICP (mm Hg) 18.7 ± 1.4 18.6 ± 1.2 0.96MICP (mm Hg) 17.2 ± 1.7 17.5 ± 1.2 0.75DICP (mm Hg) 16.5 ± 2.1 16.9 ± 1.3 0.67SCerPP (mm Hg) 107 ± 5 108 ± 5 0.60MCerPP (mm Hg) 90 ± 5 92 ± 6 0.51DCerPP (mm Hg) 81 ± 6 83 ± 7 0.53Arterial lactate (mmol L−1) 0.9 ± 0.1 0.9 ± 0.2 0.43

MCC, miniaturized chest compressor; MAP, mean aortic pressure; SICP, systolicibp

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Table 2Cardiopulmonary resuscitation outcomes.

MCC Thumper p

ROSC 7/7 5/6 0.46Duration of CPR (min) 5.1 ± 0.4 7.0 ± 4.0 0.24Number of shocks to ROSC 1.0 ± 0.0 2.0 ± 2.0 0.21Epinephrine dosage (mg) 0.86 ± 0.26 1.46 ± 1.37 0.28Incidence of recurrent VF 1.4 ± 2.3 9.2 ± 8.7 0.04Chest compression depth (cm) 3.8 ± 0.5 5.7 ± 0.6 <0.001Rib fracture (n) 1.1 ± 1.1 3.5 ± 1.5 0.007

MCC, miniaturized chest compressor; ROSC, restore of spontaneous circulation; CPR,

for establishing ROSC were observed in the MCC group than in theThumper group. The incidence of recurrent VF was significantlylower in the animals receiving the MCC (Table 2).

ntracranial pressure; DICP, diastolic ICP; MICP, mean ICP; SCerPP, systolic cere-ral perfusion pressure; DCerPP, diastolic CerPP; MCerPP, mean CerPP. Values areresented as mean ± SD. p < 0.05 was considered significant.

.5 for the second 30 min and 0.21 thereafter. At the end of the 2 host-resuscitation, the animals were then euthanized with an intra-enous injection of 150 mg/kg sodium pentobarbital. A necropsyas routinely performed for documentation of possible injuries

o the bony thorax and thoracic and abdominal viscera resultingrom the surgical or CPR intervention or the presence of obfuscatingiseases.

.3. Measurements

Aortic and right atrial pressures, ICP, electrocardiogram andTCO2 values were continuously recorded on a PC-based data-cquisition system supported by WINDAQ software (DATAQ,kron, OH). Baseline and post-resuscitation MAP were calculateds (systolic aortic pressure (SAP) + 2× diastolic aortic pressureDAP))/3. During CPR, MAP was calculated as (SAP + DAP)/2 due tohe 50% duty cycle. CorPP was calculated as the difference betweenecompression diastolic aortic and time-coincident right atrialressures. CerPP was calculated by the following three ways: (1)aximum SAP minus coincident ICP; (2) end-diastolic aortic pres-

ure minus diastolic ICP; (3) MAP minus mean ICP.8 Intrathoracicressure and compression depth were measured in real time duringPR. Aortic blood pH, PCO2, PO2, hemoglobin and lactate concen-rations were measured at baseline and hourly after resuscitationn 200 �L aliquots of blood with a Stat Profile pHOx Plus L analyzerModel PHOXplusL; Nova Biomedical Corporation, Waltham, MA).

.4. Statistical analysis

Continuous variables were presented as mean ± SD when dataere normally distributed or as a median (25th, 75th percentiles)hen data were not normally distributed. Normal distributionas confirmed with the Kolmogorov–Smirnov test. Variables were

ompared with parametric Student’s t test or the Mann–Whitney test for nonparametric data. Comparisons between time-basedeasurements within each group were performed with a paired

ample of Student’s t test. For the comparison of categorical vari-bles such as ROSC, Fisher’s exact test was used. A value of p < 0.05as considered significant.

. Results

There were no significant differences in baseline heart rate, MAP,TCO2, ICP, CerPP and arterial lactate concentration between the

wo groups (Table 1).

During CPR, significantly lower chest compression depth wasequired to achieve the threshold level of CorPP in the MCC groupTable 2). Significantly greater intrathoracic positive pressure

cardiopulmonary resuscitation; VF, ventricular fibrillation. Values are presented asmean ± SD. p < 0.05 was considered significant.

during the compression phase of CPR was generated by the MCCdevice when compared with the Thumper device. Similarly, theMCC generated significantly greater intrathoracic negative pres-sure, which is likely due to full recoil of the chest wall during thedecompression phase (Fig. 1). Significantly better CorPP and ETCO2were achieved in the MCC group than in the Thumper group (Fig. 2).

During CPR, greater systolic and mean ICP was observed withthe MCC device. However, the difference was not statistically sig-nificant between the two groups. Interestingly, significantly lowerdiastolic ICP was achieved in the MCC group when compared to theThumper group (Fig. 3).

During CPR, significantly greater systolic and mean CerPP wereobserved in the MCC group, even the systolic and mean ICP waslower in the Thumper group. Meanwhile, the MCC device also pro-duced significantly greater diastolic CerPP than the Thumper device(Fig. 4). In addition, the administration of epinephrine during CPRresulted in greater increases in CorPP and CerPP in both groups;while greater ICP was also observed in all animals after the injectionof epinephrine.

Finally, seven animals in the MCC group were successfully resus-citated. However, only five of the six animals were resuscitatedin the Thumper group. In addition, shorter duration of CPR, lessepinephrine dosage and the number of shocks that were required

Fig. 1. The intrathoracic pressure during cardiopulmonary resuscitation (CPR). MCC,miniaturized chest compressor. #p < 0.05, *p < 0.01 vs. Thumper group.

686 J. Xu et al. / Resuscitation 85 (2014) 683–688

Fig. 2. The coronary perfusion pressure and end-tidal carbon dioxide during car-dcv

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iopulmonary resuscitation (CPR). MCC, miniaturized chest compressor; CorPP,oronary perfusion pressure; ETCO2, end-tidal carbon dioxide. #p < 0.05, *p < 0.01s. Thumper group.

At necropsy, significantly less rib fractures were observed inhe animals treated with the MCC device than the Thumper deviceTable 2).

. Discussion

The present study demonstrated that chest compression withhe MCC generated significantly greater intrathoracic positive and

ig. 3. The systolic, diastolic and mean intracranial pressure during cardiopul-onary resuscitation (CPR). MCC, miniaturized chest compressor; SICP, systolic

ntracranial pressure; DICP, diastolic ICP; MICP, mean ICP.p < 0.05, *p < 0.01 vs. Thumper group.

Fig. 4. The systolic, diastolic and mean cerebral perfusion pressure during car-diopulmonary resuscitation (CPR).

MCC, miniaturized chest compressor; SCerPP, systolic cerebral perfusion pressure;DCerPP, diastolic CerPP; MICP, mean CerPP. #p < 0.05, *p < 0.01 vs. Thumper group.

negative pressures during CPR. Consequently, significantly betterCorPP and ETCO2 were achieved in the animals receiving the MCC.Though the MCC caused indistinguishably greater increases in sys-tolic and mean ICP, the systolic and mean CerPP were significantlyimproved when compared with the Thumper device. In addition,diastolic ICP and CerPP were significantly better in the MCC groupthan in the Thumper group.

The structure of the MCC device has been described in detail byour previous study.9 The functional mechanisms of this device arebased on both the cardiac and thoracic pump theories. Kouwen-hoven et al. demonstrated that external chest compression mightresult in forward blood flow by squeezing the ventricles betweenthe sternum and the spine, which was known as the “cardiacpump mechanism”.10 Subsequently, Rudikoff et al. developed the“thoracic pump mechanism” and thought that the intrathoracicpressure generated during CPR was responsible for the generationof blood flow.11 Currently, both mechanisms are accepted to berelevant.

In the present study, the MCC device compressed the heartdirectly by a piston and also the bony thorax directly by a torsorestraint so that both of the two mechanisms might be exerted.Even if the compression depth during CPR was significantly lowerin the MCC group, significantly greater intrathoracic positive pres-sure was generated by the MCC. Similarly, full and quick chestrecoil was accomplished through the timely retreat of piston andthe remaining tension of the torso restraint during the decom-pression phase; this resulted in significantly greater intrathoracicnegative pressure. Finally, significant improvement of myocardial

perfusion and flow indicated by significantly better CorPP andETCO2 was achieved in the MCC group, which resulted in theincrease of successful resuscitation. In addition, significantly less

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horacic injury such as rib fractures were observed in the MCCroup, mainly due to the low compression depth and the sta-ilization provided by the torso restraint which served as a ribelt.

Cerebral perfusion during CPR is a major determinant of the neu-ologic outcome of CA victims. One of the major goals of CPR is torovide adequate cerebral perfusion and facilitate the neurologicalecovery after resuscitation. However, the increase in intrathoracicositive pressure during chest compression also causes the simul-aneous increases in both MAP and ICP. The conduction of pressuresetween intrathoracic pressure and MAP or ICP is complicated and

nfluenced by multiple factors. Thus, it is doubtful that whetherhe elevation of intrathoracic pressure would improve cerebralerfusion and flow. In an earlier dog model of CPR, Safar P et al.emonstrated that CerPP kept relatively unchanged following the

ncrease of intrathoracic pressure.12 Koehler RC et al. applied SCV-PR (simultaneous ventilation at high airway pressure with everyhest compression combined with abdominal binding) in dogs andound that significantly greater CerPP and cerebral blood flow werechieved when compared with conventional CPR.13 Guerci AD et al.nvestigated the mechanisms of transmission of intrathoracic pres-ure to intracranial space and concluded that the transmission ofntrathoracic pressure during CPR might be conducted through thepinal subarachnoid fluid space via thoracic intervertebral foram-na and the non-valved epidural veins. Furthermore the changes inCP were approximately one third of the changes in intrathoracicressure.14 In the present study, chest compression performed byhe MCC achieved a significantly greater increase in calculatederPP with only a mild increase in systolic and mean ICP dur-

ng CPR when compared with the Thumper device. However, theiastolic ICP produced during the decompression phase of chestompression was significantly decreased in the animals receivinghe MCC.

Although mechanical CPR is attractive, current evidence is stillnsufficient for the use of mechanical CPR in the clinical setting.arly animal studies demonstrated that mechanical CPR signifi-antly improved myocardial and cerebral blood flow and thereforeurvival when compared with manual CPR.15–18 Recently, the proofrom several human observational studies also showed beneficialutcomes of CPR following mechanical chest compression.19–21

urrently, AHA guidelines recommend that mechanical CPR couldnly be considered for use by properly trained personnel in thepecific setting of CA that makes manual CPR difficult.22 The MCC,s a novel device developed by our group, has shown its effective-ess in the performance of mechanical chest compression in animaltudies and preliminary human studies.9,23,24 It may provide a newhoice for mechanical CPR.

. Limitations

There were certain limitations in our study. First, we did notirectly measure the changes of cerebral blood flow during CPR.hus, the calculated CerPP might to some extent cause the devi-tion for indicating the level of cerebral blood flow. Second, thepinephrine was used in this study due to its improvement in CorPPy alpha1- and alpha2-adrenergic activity so as to re-establishpontaneous circulation. However, previous studies have demon-trated that administration of epinephrine during CPR might resultn the decreases in cerebral cortical microcirculatory blood flownd also carotid blood flow.9,25 In this study, since the concurrent

ncreases in both CerPP and ICP were achieved after administra-ion of epinephrine, whether the MCC device could cause furtherncrease in cerebral blood flow during CPR is unknown. Third, the

echanism of pressure transmission requires further investigationn this MCC device.

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6. Conclusions

Mechanical chest compression with the MCC significantlyimproved calculated CerPP but did not compromise ICP during CPRin a porcine model of CA.

Conflict of interest statement

Dr Tang is one of the inventors of the miniaturized mechanicalchest compressor device. None of the other authors or the WeilInstitute has commercial interests in the device.

Acknowledgements

Lisa Luna contributed to the editing of this manuscript. JenaCahoon contributed to the research of this manuscript.

Appendix A. Supplementary data

Supplementary data associated with this article can be found,in the online version, at http://dx.doi.org/10.1016/j.resuscitation.2014.01.014.

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