- Original research
- Open Access
Load-distributing-band cardiopulmonary resuscitation for out-of-hospital cardiac arrest increases regional cerebral oxygenation: a single-center prospective pilot study
© Ogawa et al. 2015
- Received: 3 February 2015
- Accepted: 7 November 2015
- Published: 14 November 2015
Despite advances in therapeutic strategies and improved guidelines, morbidity and mortality rates for out-of-hospital cardiac arrest (OHCA) remain high. Especially, neurological prognosis is one of the most important problems even though brain protection therapy for patients with OHCA has improved greatly in recent years due to the development of emergency post-cardiac arrest interventions such as mild therapeutic hypothermia, early percutaneous coronary intervention, and extracorporeal cardiopulmonary resuscitation (CPR). Recently, cerebral regional oxygen saturation (rSO2) has received attention as a method for evaluation of cerebral oxygenation. We have reported that conventional chest compression did not improve the rSO2 of cardiac arrest patients if they did not achieve return of spontaneous circulation. It is, however, unclear whether a mechanical CPR device is helpful in improving rSO2. The purpose of this study was to evaluate the effects of load-distributing-band CPR (LDB-CPR) on rSO2.
In this prospective study, LDB-CPR was begun for OHCA with the AutoPulseTM device on patient arrival at hospital. During mechanical CPR, rSO2 values were recorded continuously from the forehead of the patients. CPR for patients with OHCA was performed according to the Japan Resuscitation Council Guidelines 2010 except for using the AutoPulseTM instead of manual chest compression.
From December 2012 to December 2013, 34 patients (mean age, 75.6 ± 12.8 years) with OHCA were included in this study. Duration of time from recognition of cardiac collapse to arrival to hospital was 31.0 ± 11.4 min. Compared with the rSO2 value of 38.9 ± 0.7 % prior to starting LDB-CPR, rSO2 values at 4, 8 and 12 minutes increased significantly after initiation of LDB-CPR (44.0 ± 0.9 %, 45.2 ± 0.8 %, and 45.5 ± 0.8 %, respectively, p < 0.05).
LDB-CPR significantly increased the rSO2 of cardiac arrest patients during resuscitation.
Sudden cardiac arrest is a leading cause of death and remains a major public health problem in the industrialized world . Despite improvements in resuscitation practice including the ‘chain of survival’, outcomes from out-of-hospital cardiac arrest (OHCA) remain poor [2, 3]. Especially, neurological prognosis is one of the most important problems even though brain protection therapy for patients with OHCA has greatly improved in recent years due to the development of emergency post-cardiac arrest interventions such as mild therapeutic hypothermia, early percutaneous coronary intervention, and extracorporeal cardiopulmonary resuscitation (CPR) . For cerebral resuscitation, it is important to maintain cerebral oxygenation during CPR. However, only a few reports have evaluated cerebral oxygenation, and there is no effective way of maintaining cerebral oxygenation with manual CPR.
Previous reports have noted that an inadequate intraoperative value of cerebral regional oxygen saturation (rSO2) is a significant predictor of postoperative neurological complications after cardiovascular surgery [5, 6]. Now, rSO2 can be measured noninvasively in real time by near-infrared spectroscopy (NIRS). NIRS does not require vascular pulsation and can measure rSO2 even in patients with hypotension, hypothermia, and/or circulatory arrest. rSO2 on hospital arrival is a potential novel predictor of neurological outcomes at hospital discharge in patients with OHCA.
Therefore, high-quality chest compressions are emphasized by the International Liaison Committee on Resuscitation (ILCOR) . Mechanical chest compression devices have been developed to assist rescuers in providing consistent high-quality compressions. A mechanical chest compression device that uses a load-distributing band (LDB) has been shown in animal and human studies to improve hemodynamic parameters over that of manual CPR [8, 9]. The results show that the ability to achieve return of spontaneous circulation (ROSC) with mechanical chest compression devices is significantly improved when compared with manual chest compressions. Therefore, the purpose of this study was to evaluate both the changes of rSO2 during CPR and the effects of LDB-CPR on rSO2.
Osaka University Hospital, with one of the largest emergency departments in western Japan, services approximately 1 million people who reside in a 200-km2 area in the suburbs, which includes a number of high-rise condominiums and some mountainous regions. The population density is approximately 10,910 persons per km2, and there are 27 fire stations with a corresponding number of emergency dispatch centers. Emergency medical services (EMS) at these fire stations are provided by municipal governments. EMS personnel are trained in all aspects of advanced life support procedures for prehospital emergency care.
We performed a single-center prospective pilot study that included patients with OHCA transferred to the emergency room of Osaka University Hospital from December 2012 to December 2013. The exclusion criteria included a patient age of <15 years and OHCA caused by trauma.
The study protocol complied with the guidelines for epidemiologic studies issued by the Ministry of Health, Labour and Welfare of Japan and was approved by the Ethical Committee at Osaka University (no. 12385). Every patient received the standard care available at the hospital, and no patient received any experimental intervention. In light of these safeguards, the Ethical Committee approved this study and permitted the study to be exempt from the acquisition of oral or written consent.
All patients underwent conventional CPR with manual chest compressions delivered by EMS personnel with or without bystander CPR. After arriving at the hospital, the patients underwent conventional CPR with manual chest compressions delivered by the medical staff until LDB-CPR was started. We could not evaluate the prehospital or in-hospital quality of conventional CPR with manual chest compression. We began to measure the rSO2 of the patients with the NIRS device (TOS-OR; Fujita Medical Co., Tokyo, Japan) when they arrived in the emergency room. Patients underwent LDB-CPR by mechanical chest compression delivered by the AutoPulseTM system (ZOLL, Chelmsford, MA, USA) if they were intubated prior to hospital arrival. Patients who were not intubated at the time of hospital arrival were administered LDB-CPR from 4 minutes after intubation to exclude the effect of oxygenation by intubation. Rhythm analysis and pulse check were performed every second minute. If the rhythm was shockable, defibrillation was performed during LDB-CPR.
The AutoPulseTM system is a portable chest compression device constructed around a backboard that contains a motor that retracts a load-distributing band under microprocessor control. The band is connected to a shaft in the board. The band is tightened and loosened around the chest by the motor, which alternates the rotation of the shaft in both directions. The patient is positioned on the board, and the two broad ends of the band are placed around the patient’s chest and connected to each other. The length of the band automatically adjusts to the size and the shape of the patient. The microprocessor is programmed to provide a constant 20 % reduction in the anterior-posterior dimension of the individual patient’s chest during the compression phase. The compression rate is 80 ± 5 min-1 with equal periods of compression and unloading, and the device can be operated in a continuous compression mode or in a 15:2 mode. In the 15:2 mode, compressions stop for 3 s after every 15 have been applied to allow two ventilations to be given to the patient. In this study, all resuscitation attempts were performed in the continuous compression mode. LDB-CPR treatment was continued until ROSC or death was declared.
An NIRS device was prepared for operation before patient arrival at the hospital. Upon patient arrival, the patient’s skin was thoroughly cleaned, and the sensor was carefully applied to the patient’s forehead. The rSO2 values stabilized within several seconds after placement of the NIRS probes. The rSO2 values were then monitored during CPR, and the values measured at each of the points the pulse was checked were used for analysis. The normal range of cerebral rSO2 was determined to be over 60 % for the following reasons. First, the oxygen saturation of arterial blood is nearly 100 % and that of venous blood is 50-60 %. Assuming that the arterial blood occupies about one fourth of the tissue blood volume, the mean oxygen saturation in the tissue is estimated to be 60-70 %. When the arterial blood supply is interrupted, oxygen is consumed and the rSO2 drops to that of venous blood, around 60 %, and anaerobic metabolism begins. The rSO2 actually shows a biphasic decline when arterial perfusion is interrupted: rSO2 initially drops rapidly, and then the slope becomes more gradual. Second, the lower normal limit of oxygen saturation that is commonly accepted in monitoring of jugular vein blood is 55 %. Third, the lower limit of oxygen saturation of mixed venous blood is 60 %. Fourth, the range of cerebral rSO2 from 15 volunteers (43.2 ± 8.9 years, 10 men and 5 women) breathing room air was 71.2 ± 3.9 %. Finally, a cardiovascular surgery study suggested that the occurrence of neurological events increased when a drop in rSO2 of below 60 % was sustained for a long period in elderly people . Clinical staff performed routine post-cardiac arrest interventions regardless of these measurements. All patients were treated principally according to the strategy of the Japan Resuscitation Council 2010 Guidelines.
After the patients were entered into the study, their rSO2 values were measured until ROSC, or LDB-CPR was stopped. The variables of age, sex, and time from the emergency call to arrival at hospital were assessed. We evaluated patient rSO2 values pre-LDB-CPR and at 4, 8, and 12 min after the start of LDB-CPR for any cause. Neurological prognosis was evaluated with the Cerebral Performance Category (CPC) score. The presence of any serious adverse events related to LDB-CPR was recorded.
The comparison of rSO2 values was analyzed by analysis of variance adjusted for the pre-rSO2 values as a covariate and by the Dunnett test. A p value of less than 0.05 was considered to indicate statistical significance. Statistical analyses were performed with JMP Pro version 10.0.2 for Macintosh (SAS Institute Inc., Cary, NC, USA).
Age, mean±SD, years
Sex, n (male/female)
Bystander/witness status, n
No bystander with witness
Initially documented rhythm at scene of cardiac arrest, n
Time from call to hospital arrival, mean±SD, min
Intubation by EMS personnel, n
Rhythm at rSO2 measurement, n
Return of spontaneous circulation, n
Of the 13 patients with ROSC, only one patient survived to hospital discharge with a CPC score of 2. The remaining 12 patients either died or survived to hospital discharge with a CPC score of 5. There were no complications caused by LDB-CPR in this study.
In this study, LDB-CPR increased rSO2 values compared with manual CPR, and rSO2 values were maintained during LDB-CPR. In our previous study, manual chest compression could not increase rSO2 without ROSC . Halperin et al. reported that LDB-CPR improved hemodynamics over manual CPR and produced pre-arrest levels of cerebral flow with epinephrine in a pig model . Duchateau et al. reported that a significant improvement in hemodynamics was observed during CPR when the AutoPulseTM automated chest compression device was used compared to the manual active compression-decompression CPR in patients with OHCA . We believe that the increase in rSO2 values during LDB-CPR was effected by the hemodynamic improvement brought about by the AutoPulseTM.
Kämäräinen et al. showed that the rSO2 value could not be improved by manual chest compression CPR with a feedback device . In the present study, the rSO2 value pre-LDB-CPR, which reflected the value resulting from prehospital manual chest compression, was very low (38.9 ± 0.7 %), indicating that manual chest compression could not increase the rSO2 value. Several studies have found an increase in rSO2 after ROSC in patients. The rSO2 values also increased significantly in our non-ROSC patients, which may mean that LDB-CPR has effects that increase the rSO2 without affecting ROSC.
Hock Ong et al. reported that a resuscitation strategy using LDB-CPR in an emergency department environment was associated with improved neurologically intact survival on discharge in adults who experienced non-traumatic cardiac arrest . Although it is important to maintain the rSO2 value to improve the neurological prognosis, in the present study, the neurological prognosis was very poor. As a possible reason, the time from the emergency call to hospital arrival was very long. This could be a result of the long distances and times experienced in transferring the patients living in the mountainous regions or high-rise condominiums. The changes in rSO2 values may relate to transfer distance or time. Because the rSO2 value was maintained by LDB-CPR, the neurological prognosis might have been improved if LDB-CPR had been initiated in the prehospital setting. We have just begun to study the prehospital changes in rSO2 values to help resolve this important problem.
In the CIRC trial, compared to manual CPR, LDB-CPR resulted in statistically equivalent survival and neurological prognosis to hospital discharge after OHCA of presumed cardiac origin . The different findings between the present study and the CIRC trial could be influenced by the differences in the strategy of the resuscitation guidelines. The Japan Resuscitation Council 2010 Guidelines recommend manual CPR only. In the present study, 8 patients were intubated prior to hospital arrival. Although LDB-CPR in patients who were not intubated at the time of hospital arrival was begun from 4 minutes after intubation to exclude the effect of oxygenation by intubation, it is possible that the rSO2 values were increased by intubation. It is thus necessary to evaluate rSO2 values without intubation between manual CPR and LDB-CPR.
The use of mechanical chest compression devices for CPR remains controversial. A previous meta-analysis showed that the ability to achieve ROSC with mechanical chest compression devices is significantly improved when compared with manual chest compression . In our study, LDB-CPR increased and maintained rSO2 values during resuscitation. We think that LDB-CPR may offer a significant beneficial effect on the maintenance of cerebral oxygenation during resuscitation. Moreover, we have developed a portable NIRS system and conducted a pilot study of the device . This will allow us to evaluate changes in rSO2 resulting from prehospital mechanical chest compression.
We recognize several limitations in this study. First, the present study is an observational and not a randomized control study. For obvious reasons, this study could not be blinded, and it was difficult to randomize in the prehospital stage. Therefore, we acknowledge the necessity of comparing the changes in rSO2 values between conventional CPR with manual chest compression and LDB-CPR in the prehospital stage. Second, this is a single-center study, and third, the sample size was small. But the present study was a pilot study. It was exploratory and for this reason, the objective was 30 patients included (which has been achieved). The final limitation was that the prehospital or in-hospital quality of conventional CPR with manual chest compression could not be evaluated. There are some systems/devices that do not monitor the quality of CPR. None of these systems have been used in this study. The combination of these limitations might cause multiple unmeasured variables to account for the outcome differences observed in this study.
LDB-CPR significantly increased the rSO2 of patients with OHCA. LDB-CPR may have an important beneficial effect on the maintenance of cerebral oxygenation during resuscitation.
This work was supported by Grants-in-Aid for scientific research from the Ministry of Education, Culture, Sports, Science, and Technology in Japan (nos. 24390401 and 15H05007).
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