Abstract
Background
The prognosis of non‐shockable out‐of‐hospital cardiac arrest is worse than that of shockable out‐of‐hospital cardiac arrest. We investigated the associations between the etiology and prognosis of non‐shockable out‐of‐hospital cardiac arrest patients who experienced the return of spontaneous circulation after arriving at hospital.
Methods and Results
All subjects were extracted from the SOS‐KANTO 2012 study population. The subjects were 3,031 adults: (i) who had suffered out‐of‐hospital cardiac arrest, (ii) for whom there were no pre‐hospital data on ventricular fibrillation/pulseless ventricular tachycardia until arrival at hospital, (iii) who experienced the return of spontaneous circulation after arriving at hospital. We compared the patients' prognosis after 1 and 3 months between various etiological and presumed cardiac factors. The proportion of the favorable brain function patients that developed pulmonary embolism or incidental hypothermia was significantly higher than that of the patients with presumed cardiac factors (1 month, P < 0.0001 and P < 0.0001, respectively; 3 months, P = 0.0018 and P < 0.0001, respectively). In multiple logistic regression analysis, pulmonary embolism and incidental hypothermia were found to be significant independent prognostic factors for 1‐ and 3‐month survival and the favorable brain function rate.
Conclusions
In patients who suffer non‐shockable out‐of‐hospital cardiac arrest, but who experience the return of spontaneous circulation after arriving at hospital, the investigation and treatment of pulmonary embolism as a potential etiology may be important for improving post‐resuscitation prognosis.
Keywords: Cardiopulmonary arrest, cardiopulmonary resuscitation, non‐shockable OHCA, out‐of‐hospital cardiac arrest (OHCA), pulmonary embolism
Background
The frequency of the return of spontaneous circulation (ROSC) is lower after non‐shockable out‐of‐hospital cardiopulmonary arrest (non‐shockable OHCA), such as pulseless electrical activity (PEA) and asystole, than after ventricular fibrillation (VF)/pulseless ventricular tachycardia (VT)‐related shockable out‐of‐hospital cardiopulmonary arrest (shockable OHCA), and hence, non‐shockable OHCA exhibits a worse prognosis.1, 2 It has been suggested that early electrical defibrillation might be important for achieving ROSC after shockable OHCA.2 After ROSC, it is relatively easy to determine whether a cardiac arrest has been caused by a disease with a clear VF‐/pulseless VT‐associated mechanism, such as acute coronary syndrome (ACS), long QT syndrome, and various electrolyte abnormalities, and it has been suggested that etiology‐based treatment might lead to improvements in the prognosis of cardiac arrest patients.3
Whereas electrical defibrillation is used to treat shockable OHCA, there are no specific treatments for the management of non‐shockable OHCA. Therefore, to restore the heart beat and improve prognosis, in many cases it might be necessary to investigate/overcome the cause of the cardiopulmonary arrest.2, 4 As few diagnostic procedures can be carried out during cardiopulmonary resuscitation (CPR), it might be impossible to identify the etiology of non‐shockable OHCA, except in cases in which the etiology is initially clear, such as those involving trauma or suffocation, which would affect the chance of the ROSC being achieved.
In addition, even after ROSC has occurred, non‐shockable OHCA itself is not indicative of particular etiological factors; therefore, the underlying causes of OHCA should be investigated to aid treatment.4 In the 2010 resuscitation guidelines, it is recommended that therapeutic hypothermia and early reperfusion therapy for ST‐segment elevation myocardial infarction should be carried out during post‐advanced cardiovascular life support–resuscitation care.5 However, it is unclear whether these procedures are sufficient in patients with non‐shockable OHCA, whose etiologies can differ.
As specific etiology‐based treatments might improve prognosis, it is important to examine the associations between etiology and prognosis in patients with non‐shockable OHCA based on current treatments. Accordingly, patients in whom the etiology of non‐shockable OHCA cannot be definitively determined might have a poor prognosis.
The purpose of this study was to clarify the association between the causes of non‐shockable OHCA and prognosis after 1 and 3 months in patients who had ROSC after suffering a non‐shockable OHCA compared with unknown etiology.
Methods
Study design
The present study analyzed the data from the SOS‐KANTO 2012 study. The SOS‐KANTO 2012 study was a prospective survey that aimed to collect the pre‐/in‐ hospital data and follow‐up records of cardiac arrest patients who were admitted to 67 emergency hospitals in the Kanto region between January 2012 and March 2013.6 This study was approved by the institutional review boards of all 67 institutions, which waived the requirement for informed patient consent to ensure the anonymity of the participants, which is stipulated in the guidelines for such studies produced by the Japanese government.6
Subjects
Of 16,452 patients for whom 3‐month prognostic data were collected in the SOS‐KANTO 2012 study, we excluded those who were aged 17 years or younger, those who suffered in‐hospital cardiopulmonary arrest, those that were shocked with an automated external defibrillator by a bystander, those with cardiopulmonary arrest in whom there were records on VF/pulseless VT or electric shock by the emergency medical staff until arrival to hospital, those in whom ROSC was achieved until arrival, and those in whom the ROSC was not achieved after arrival, which resulted in 3,031 patients being included in this study (Fig. 1). Diagnostic procedures for identifying the etiology of cardiopulmonary arrest might have been carried out more thoroughly in patients in whom the ROSC was achieved. Thus, this study only included patients in whom the ROSC was achieved after arrival for non‐shockable OHCA.
Figure 1.
Selection of study subjects. Of 16,452 patients for whom 3‐month prognostic data were collected in the SOS‐KANTO 2012 study, 3,031subjects were extracted for this study after excluding those who were aged 17 years or younger, those who suffered an in‐hospital cardiopulmonary arrest, those who were shocked with an automated external defibrillator (AED) by a bystander, those with cardiopulmonary arrest in whom there were records on pulseless ventricular tachycardia (VT)/ventricular fibrillation (VF) or electric shocks until arrival to hospital, those in whom the return of spontaneous circulation (ROSC) occurred before their arrival at hospital, and those in whom ROSC was not achieved after arrival. The numbers of patients that were followed‐up at 1 and 3 months and that showed each etiological factor are shown. OHCA, out‐of‐hospital cardiac arrest.
Definitions and data collection
Cardiac arrest was defined as the cessation of cardiac mechanical activity; that is, the absence of a detectable pulse, responsiveness, and normal breathing.7, 8 All cardiac arrest patients who were transported to the participating hospitals by emergency medical service (EMS) providers were included in the SOS‐KANTO 2012 study.6 Pre‐ and in‐hospital treatments were generally delivered by EMS personnel, physicians, and other healthcare providers in line with the national guidelines of the Japan Resuscitation Council, which are based on the international guidelines.9 The EMS providers collected pre‐hospital information in the standardized Utstein style:7, 8 the sex and age of the patients, the initial cardiac rhythm, and the time course of resuscitation. The latter included the time at which CPR was started by a bystander or EMS, the presence or absence of VF/pulseless VT, whether electrical shocking was carried out by the EMS providers, and the time of arrival at hospital. Additional information including whether the cardiac arrest was witnessed by a bystander, whether a bystander initiated CPR, and whether spontaneous circulation was restored before the patient arrived at hospital was also collected. The quality of CPR could not be assessed.
The causes of cardiac arrest were determined by the attending physicians caring for the patients in accordance with the SOS‐KANTO 2012 survey form, which was produced in the standardized Utstein style.7, 8 According to this classification, the patients were diagnosed with cardiac arrest due to a presumed cardiac factor (PCF) unless an obvious non‐cardiac etiology, acute coronary syndrome (ACS), or a definite cardiogenic factor other than ACS was observed. So, patients that suffered cardiac arrests with no definitive etiology were classified into the PCF group. Non‐cardiac etiologies were classified into extrinsic non‐cardiogenic factors (trauma, burns, incidental hypothermia, hanging, drowning, suffocation, and poisoning), intrinsic non‐cardiogenic factors (pulmonary embolism, acute aortic dissection, aortic aneurysmal rupture, subarachnoid hemorrhaging, and bronchial asthma), and other non‐cardiogenic factors, including many minor etiological factors (e.g., sepsis, anaphylaxis).
Neurological outcomes were evaluated and reported using the Cerebral Performance Categories (CPC) scale, and responses were scored as follows: category 1, good cerebral performance; category 2, moderate cerebral disability; category 3, severe cerebral disability; category 4, coma/vegetative state; category 5, brain death/death.7, 8, 10
Classification and analysis of each etiological factor and prognosis
The subjects were grouped based on the etiological factors for cardiopulmonary arrest identified by the attending physicians after arrival according to the abovementioned SOS‐KANTO 2012 Study classification (Fig. 1). The 1‐ and 3‐month survival rates (CPC 1–4) and the proportion of patients who had favorable brain function (CPC 1–2) at these time points were compared between each group and a group of patients who showed PCF, but whose etiologies were unclear. In addition, multiple logistic regression analysis was carried out using the background and etiological factors as explanatory variables.
Statistics
We used StatFlex version 6.0 (Artech, Osaka, Japan) for all statistical analyses. Continuous variables are expressed as mean ± SD values, and were compared using the Mann–Whitney U‐test. When comparing discrete variables between two groups, the χ2‐test was used, and Fisher's exact test was used when the number of samples was low. The independency of prognostic predictors was tested using multiple logistic regression analysis. P‐values of <0.05 were regarded as statistically significant.
Results
In total, 3,031 patients were included in this study (Fig. 1), and the subjects' background data are presented in Table 1. The results of analyses are presented in Figures 2 and 3. The 1‐ and 3‐month survival rates of the incidental hypothermia group were significantly higher than those of the PCF group, respectively (1 month: 50.0 vs. 3.1%, respectively, P < 0.0001; 3 months: 35.7 vs. 1.8%, respectively, P < 0.0001) (Fig. 2). In addition, body temperature on arrival at hospital were significantly lower in incidental hypothermia group than in others (26.8 ± 3.2°C vs. 35.1 ± 1.9°C, P < 0.0001). The 1‐month survival rate of the suffocation group was significantly higher than that of the PCF group (5.8 vs. 3.1%, respectively, P = 0.0170) (Fig. 2). Concerning intrinsic non‐cardiogenic factors, the 1‐ and 3‐month survival rates of the pulmonary embolism group were significantly higher than those of the PCF group (1 month: 25.0 vs. 3.1%, respectively, P < 0.0001; 3 months: 15.0 vs. 1.8%, respectively, P = 0.0002) (Fig. 2). The proportions of patients who maintained favorable brain function at 1 and 3 months were significantly higher in the incidental hypothermia group than in the PCF group (1 month: 28.6 vs. 0.6%, respectively, P < 0.0001; 3 months: 28.6 vs. 0.4%, respectively, P < 0.0001) (Fig. 3). In the pulmonary embolism group, the proportions of patients who maintained favorable brain function after 1 and 3 months were also significantly higher than in the PCF group (1 month: 15.0 vs. 0.6%, respectively, P < 0.0001; 3 months: 7.5 vs. 0.4%, respectively, P = 0.0018) (Fig. 3).
Table 1.
Background data of subjects extracted from the SOS‐KANTO 2012 study population
| Number of patients | 3,031 |
| Age, years | 73.0 ± 15.5 |
| Female/male ratio | 0.69 |
| Presence of a witness | 1,934 (63.8%) |
| CPR performed by a bystander | 1,096 (36.2%) |
| Interval from the start of CPR by a bystander or EMS until arrival, min | 22.1 ± 9.2 |
| Interval from arrival until the ROSC, min | 15.6 ± 11.5 |
| 1‐month survival | 124 (4.1%) |
| CPC 1–2 after 1 month | 33 (1.1%) |
| 3‐month survival | 70 (2.3%) |
| CPC 1–2 after 3 month | 27 (0.9%) |
Data are shown as absolute values, mean ± SD values, or ratios. CPC, Cerebral Performance Categories; CPR, cardiopulmonary resuscitation; EMS, emergency medical service; ROSC, return of spontaneous circulation.
Figure 2.
Survival rate after the return of spontaneous circulation according to the etiology of non‐shockable out‐of‐hospital cardiac arrest. *P = 0.0170, **P = 0.0002, ***P < 0.0001, vs. presumed cardiac factors (PCF).
Figure 3.
Frequency of favorable brain function (a Cerebral Performance Categories scale score of 1–2) after the return of spontaneous circulation according to the etiology of non‐shockable out‐of‐hospital cardiac arrest. *P = 0.0018, **P < 0.0001, vs. presumed cardiac factors (PCF).
Table 2 shows the background data in each etiological group that was associated with significant differences in the 1‐month survival rate, the PCF group, and ACS group. Because the background factors in other etiological groups did not influence prognosis, we did not analyze them. The mean ages of the pulmonary embolism and incidental hypothermia groups were significantly younger than those of the PCF group (60.4 ± 16.9 and 66.5 ± 15.0 vs. 76.5 ± 12.7 years, respectively, P < 0.0001 and P = 0.0068, respectively). In addition, the female‐to‐male patient ratio was significantly higher in the pulmonary embolism group than in the PCF group (1.67 vs. 0.69, respectively, P = 0.0068). Furthermore, the interval from the start of CPR until arrival was significantly shorter in the pulmonary embolism and incidental hypothermia groups than in the PCF group (16.2 ± 9.3 and 15.6 ± 11.3 vs. 22.4 ± 9.0 min, respectively, P = 0.0001, P = 0.0068).
Table 2.
Relationships between background factors and etiological factors that were associated with significant differences in the 1‐month survival rate, the presumed cardiac factor (PCF) group, and acute coronary syndrome (ACS) group in patients with out‐of‐hospital cardiopulmonary arrest
| PCF (n = 962) | Incidental hypothermia (n = 14) | Suffocation (n = 450) | Pulmonary embolism (n = 40) | ACS (n = 160) | |
|---|---|---|---|---|---|
| Age, years | 76.5 ± 12.7 | 66.5 ± 15.0** | 77.3 ± 13.2 | 60.4 ± 16.9**** | 75.7 ± 12.0 |
| Female/male ratio | 0.694 | 0.750 | 0.737 | 1.667** | 0.538 |
| Presence of a witness, % | 59.7 | 35.7 | 80.4**** | 75.0 | 65.0 |
| CPR performed by a bystander, % | 35.9 | 28.6 | 48.7**** | 30.0 | 35.6 |
| Interval from the start of CPR by a bystander or EMS until arrival, min | 22.4 ± 9.0 | 15.6 ± 11.3** | 23.6 ± 9.2* | 16.2 ± 9.3*** | 21.8 ± 10.6 |
| Interval from arrival until the ROSC, min | 16.1 ± 9.9 | 22.1 ± 17.3 | 14.3 ± 8.8**** | 21.7 ± 15.9 | 17.8 ± 11.0 |
Data are shown as mean ± SD values, ratios, or percentages. *P = 0.0208, **P = 0.0068, ***P = 0.0014, ****P < 0.0001, vs. PCF. CPR, cardiopulmonary resuscitation; EMS, emergency medical service; ROSC, return of spontaneous circulation.
Results of multiple logistic regression analyses are shown in Tables 3 and 4. Age, the interval from the start of CPR until arrival, pulmonary embolism, incidental hypothermia, and suffocation were shown to be significant independent prognostic factors for the 1‐ and 3‐month survival rates after ROSC (Table 3) brain function at 1 and 3 months (Table 4).
Table 3.
Multiple logistic regression analysis of factors affecting 1‐ and 3‐month survival in patients with non‐shockable out‐of‐hospital cardiopulmonary arrest
| Explanatory variables | 1‐month survival | 3‐month survival | ||
|---|---|---|---|---|
| Odds ratio | 95% CI | Odds ratio | 95% CI | |
| Female | 1.294 | 0.866–1.934 | 1.236 | 0.726–2.105 |
| Age, Δ= +10 years | 0.853 | 0.758–0.959 | 0.796 | 0.683–0.923 |
| Presence of witness | 1.072 | 0.689–1.666 | 1.169 | 0.644–2.123 |
| CPR performed by a bystander | 0.827 | 0.540–1.267 | 0.823 | 0.466–1.454 |
| Interval from start of CPR until arrival, Δ= +5 min | 0.644 | 0.571–0.728 | 0.584 | 0.495–0.689 |
| Interval from arrival until ROSC, Δ= +5 min | 0.940 | 0.877–1.006 | 0.954 | 0.866–1.050 |
| Acute coronary syndrome | 1.835 | 0.842–4.001 | 1.655 | 0.561–4.876 |
| Pulmonary embolism | 6.094 | 2.592–14.328 | 6.160 | 2.178–17.424 |
| Incidental hypothermia | 23.050 | 6.972–76.205 | 26.807 | 7.247–99.167 |
| Suffocation | 2.582 | 1.562–4.268 | 2.810 | 1.443–5.472 |
The underlined explanatory variables are statistically significant; i.e., independent predictive variables. CI, confidence interval; CPR, cardiopulmonary resuscitation; ROSC, return of spontaneous circulation.
Table 4.
Multiple logistic regression analysis of the factors affecting favorable brain function at 1 or 3 months (Cerebral Performance Categories 1–2) in patients with out‐of‐hospital cardiopulmonary arrest
| Explanatory variables | 1‐month survival | 3‐month survival | ||
|---|---|---|---|---|
| Odds ratio | 95% CI | Odds ratio | 95% CI | |
| Female | 1.321 | 0.610–2.862 | 0.895 | 0.368–2.177 |
| Age, Δ= +10 years | 0.784 | 0.630–0.975 | 0.720 | 0.571–0.908 |
| Presence of witness | 1.463 | 0.598–3.577 | 1.261 | 0.479–3.318 |
| CPR performed by a bystander | 1.121 | 0.494–2.541 | 1.227 | 0.495–3.045 |
| Interval from start of CPR until arrival, Δ= +5 min | 0.580 | 0.458–0.736 | 0.570 | 0.436–0.745 |
| Interval from arrival until ROSC, Δ= +5 min | 1.022 | 0.887–1.178 | 1.030 | 0.882–1.203 |
| Acute coronary syndrome | 2.557 | 0.708–9.237 | 3.340 | 0.892–12.506 |
| Pulmonary embolism | 10.805 | 3.557–32.823 | 5.702 | 1.344–24.192 |
| Incidental hypothermia | 30.335 | 7.465–123.261 | 48.125 | 11.296–205.032 |
| Suffocation | 0.806 | 0.180 | 1.068 | 0.232–4.914 |
The underlined explanatory variables are statistically significant; i.e., independent predictive variables. CI, confidence interval; CPR, cardiopulmonary resuscitation; ROSC, return of spontaneous circulation.
Discussion
The prognosis of non‐shockable OHCA is worse than that of shockable OHCA.1, 2 In many cases of non‐shockable OHCA, it might be necessary to investigate and treat the etiology of the patient's condition to achieve ROSC.2, 4 In the 2010 resuscitation guidelines,5 it is recommended that hypothermia therapy and early reperfusion therapy for ST‐segment elevation myocardial infarction should be carried out during post‐advanced cardiovascular life support–resuscitation care after the ROSC. However, it is unclear whether these procedures are sufficient.
In this study, the proportions of patients who showed favorable brain function after 1 or 3 months or survived for 1 or 3 months were significantly higher among ROSC patients that suffered non‐shockable OHCA caused by pulmonary embolism or incidental hypothermia than among the PCF group, in other words, the unknown etiology group. Multivariate analysis showed that the abovementioned conditions were independent prognostic factors, as were age and the interval from the start of CPR until arrival. This suggests that non‐shockable OHCA patients should be promptly transferred to hospital and that it is useful to clarify/manage the etiology of non‐shockable OHCA even after the ROSC in order to improve patient prognosis.
However, there are some patients with non‐shockable OHCA in whom the etiology of the condition is clear based on their clinical circumstances/course after arrival. In most of these cases, extrinsic factors are involved, and etiology‐based therapy should be added to CPR, if possible, to achieve the ROSC.4 Of the etiological factors that were found to be associated with a better prognosis in this study, suffocation and incidental hypothermia might be representative conditions. In the patients that suffocated, airway management and artificial ventilation11 were performed together with CPR. In those that suffered incidental hypothermia, rewarming12 was carried out together with CPR. In addition, in patients with incidental hypothermia, the condition might help to protect the brain.11 However, in most patients with non‐shockable OHCA, the etiology of the condition is initially unclear after arrival, although it is speculated that non‐shockable OHCA is associated with intrinsic factors. To achieve the ROSC, sufficient etiological investigations and CPR should be carried out,4 but such investigations are not always straightforward.
This study involved patients with non‐shockable OHCA in whom the ROSC was achieved after arrival. However, with respect to intrinsic factors the 1‐ and 3‐month survival rates and the proportions of patients who showed favorable brain function after 1 and 3 months were significantly higher in the pulmonary embolism group than in the presumed cardiogenic group. From the results of the univariate analysis, the interval from the start of CPR by a bystander or EMS until arrival at hospital might have some effect on the prognosis of pulmonary embolism, but the multivariate analysis also showed that these parameters were independent prognostic factors. The results of this study were obtained under the 2010 guidelines for resuscitation, in which therapeutic hypothermia, the detection of acute coronary syndrome, especially ST elevation‐type myocardial infarction, and reperfusion therapy are strongly recommended for non‐shockable OHCA patients in whom ROSC and stable respiratory/circulatory state is achieved.5 If, for example, contrast‐enhanced CT under a tentative diagnosis of pulmonary embolism and subsequent thrombolytic therapy/surgical or catheter‐mediated thrombus removal are recommended for such patients, it may contribute to an improvement in the prognosis of non‐shockable OHCA patients.
Acute pulmonary embolism‐related OHCA may suddenly occur with rapid, extensive occlusion of the pulmonary vascular floor, but the circulating blood volume and oxygen content of blood may be maintained early after onset. Therefore, a favorable prognosis may be achieved by undertaking adequate resuscitation, including chest compression, and appropriate treatments, such as assisted circulation/thrombolytic therapy/surgical thrombus removal/catheter‐mediated thrombus removal.13 We also reviewed published reports on pulmonary embolism‐related cardiopulmonary arrest. Kürkciyan et al. retrospectively investigated 1,246 patients who suffered cardiac arrests and reported that pulmonary emboli were detected in 60 patients (4.8%). They indicated that 38 of the 60 patients exhibited PEA, 30 of whom were clinically diagnosed with pulmonary embolism. In addition, 15 patients underwent thrombolytic therapy, and 2 of them survived, whereas all 15 of the patients who did not undergo thrombolytic therapy died.14 Courtney et al. reported that the sensitivity and specificity of pulmonary embolism were 67.6 and 94.5%, respectively, when the condition was limited to witnessed PEA among patients with intrinsic cardiac arrest.15 In the 2010 American Heart Association Guidelines for CPR and emergency cardiovascular care, administration of fibrinolytics is recommended as class IIa in patients with cardiac arrest due to presumed or known pulmonary embolism.4 Even after ROSC, pulmonary embolism must be considered as a possible cause of cardiac arrests.
In this study, we also compared the outcomes of patients with ACS, which the 2010 resuscitation guidelines recommend should be considered as a potential etiology/treated after the ROSC,5 with those of patients with PCF. However, there was no significant difference in the prognosis of these two groups. Therefore, pulmonary embolism could be given priority over ACS, in cases of non‐shockable OHCA after ROSC.
The present study had the following limitations. First, it was a retrospective, observational study. Second, it is unclear whether the results of this study are indicative of the prognosis of all cardiopulmonary arrest patients. Third, the presence/absence of a diagnosis before ROSC might have biased the subject enrolment process. Fourth, the etiology of each cardiopulmonary arrest was evaluated by the attending physician, and no detailed information about the diagnostic process was obtained in the SOS‐KANTO 2012 study; thus, it is impossible to evaluate the accuracy/usefulness of diagnosis. Theoretically, all non‐cardiogenic and definite cardiogenic factors might be included in PCF. Thus, the fact that the identification of the etiology of non‐shockable OHCA was completely dependent on the discretion of the attending physicians is an important limitation of the present study. Finally, no data on concomitant diseases were collected, and so their influence cannot be evaluated.
Conclusion
Among patients who suffered non‐shockable OHCA and then achieved ROSC after arriving at hospital, those who suffered incidental hypothermia or pulmonary embolism had better prognoses than those in the PCF group with unknown etiology. In particular, our results obtained under the 2010 resuscitation guidelines suggest that the investigation and treatment of pulmonary embolism as a potential etiology may be important for improving patients' post‐resuscitation prognosis.
Part of this study was presented at the 42nd Annual Scientific Meeting of the Japanese Association for Acute Medicine, Fukuoka, in October 2014.
Conflicts of Interest
None.
Contributors
Toru Yoshida, Yoshihiro Masui, Yasuhiko Taira, Nobuya Kitamura, Yoshio Tahara, Atsushi Sakurai, Naohiro Yonemoto, Ken Nagao, Arino Yaguchi, and Naoto Morimura.
SOS‐KANTO 2012 Steering Council
Yokohama City University Medical Center, Kanagawa (President, Naoto Morimura MD); Nihon University School of Medicine, Tokyo (Director, Atsushi Sakurai MD); National Cerebral and Cardiovascular Center Hospital, Osaka (Director, Yoshio Tahara MD); Tokyo Women's Medical University Hospital, Tokyo (Arino Yaguchi MD); Nihon University Surugadai Hospital, Tokyo (Ken Nagao MD); Nippon Medical School Hospital, Tokyo (Tagami Takashi MD); Japanese Red Cross Maebashi Hospital, Gunma (Dai Miyazaki MD); National Disaster Medical Center, Tokyo (Tomoko Ogasawara MD); Keio University Hospital, Tokyo (Kei Hayashida MD, Masaru Suzuki MD); Tokai University School of Medicine, Kanagawa (Mari Amino MD); Kimitsu Chuo Hospital, Chiba (Nobuya Kitamura MD); Juntendo University Nerima Hospital, Tokyo (Tomohisa Nomura MD); Tokyo Metropolitan Children's Medical Centre, Tokyo (Naoki Shimizu MD); Tokyo Metropolitan Bokutoh Hospital, Tokyo (Akiko Akashi MD); National Center of Neurology and Psychiatry, Tokyo, Japan (Naohiro Yonemoto DPH).
SOS‐KANTO 2012 Study Group
Tokai University School of Medicine (Sadaki Inokuchi MD); St. Marianna University School of Medicine, Yokohama Seibu Hospital (Yoshihiro Masui MD); Koto Hospital (Kunihisa Miura MD); Saitama Medical Center Advanced Tertiary Medical Center (Haruhiko Tsutsumi MD); Kawasaki Municipal Hospital Emergency and Critical Care Center (Kiyotsugu Takuma MD); Yokohama Municipal Citizen's Hospital (Ishihara Atsushi MD); Japanese Red Cross Maebashi Hospital (Minoru Nakano MD); Juntendo University Urayasu Hospital (Hiroshi Tanaka MD); Dokkyo Medical University Koshigaya Hospital (Keiichi Ikegami MD); Hachioji Medical Center of Tokyo Medical University (Takao Arai MD); Tokyo Women's Medical University Hospital (Arino Yaguchi MD); Kimitsu Chuo Hospital (Nobuya Kitamura MD); Chiba University Graduate School of Medicine (Shigeto Oda MD); Saiseikai Utsunomiya Hospital (Kenji Kobayashi MD); Mito Saiseikai General Hospital (Takayuki Suda MD); Dokkyo Medical University (Kazuyuki Ono MD); Yokohama City University Medical Center (Naoto Morimura MD); National Hospital Organization Yokohama Medical Center (Ryosuke Furuya MD); National Disaster Medical Center (Yuichi Koido MD); Yamanashi Prefectural Central Hospital (Fumiaki Iwase MD); Surugadai Nihon University Hospital (Ken Nagao MD); Yokohama Rosai Hospital (Shigeru Kanesaka MD); Showa General Hospital (Yasusei Okada MD); Nippon Medical School Tamanagayama Hospital (Kyoko Unemoto MD); Tokyo Women's Medical University Yachiyo Medical Center (Tomohito Sadahiro MD); Awa Regional Medical Center (Masayuki Iyanaga MD); Todachuo General Hospital (Asaki Muraoka MD); Japanese Red Cross Medical Center (Munehiro Hayashi MD); St. Luke's International Hospital (Shinichi Ishimatsu MD); Showa University School of Medicine (Yasufumi Miyake MD); Totsuka Kyoritsu Hospital 1 (Hideo Yokokawa MD); St. Marianna University School of Medicine (Yasuaki Koyama MD); National Hospital Organization Mito Medical Center (Asuka Tsuchiya MD); Tokyo Metropolitan Tama Medical Center (Tetsuya Kashiyama MD); Showa University Fujigaoka Hospital (Munetaka Hayashi MD); Gunma University Graduate School of Medicine (Kiyohiro Oshima MD); Saitama Red Cross Hospital (Kazuya Kiyota MD); Tokyo Metropolitan Bokutoh Hospital (Yuichi Hamabe MD); Nippon Medical School Hospital (Hiroyuki Yokota MD); Keio University Hospital (Shingo Hori MD); Chiba Emergency Medical Center (Shin Inaba MD); Teikyo University School of Medicine (Tetsuya Sakamoto MD); Japanese Red Cross Musashino Hospital (Naoshige Harada MD); National Center for Global Health and Medicine Hospital (Akio Kimura MD); Tokyo Metropolitan Police Hospital (Masayuki Kanai MD); Medical Hospital of Tokyo Medical and Dental University (Yasuhiro Otomo MD); Juntendo University Nerima Hospital (Manabu Sugita MD); Nihon University School of Medicine (Kosaku Kinoshita MD); Toho University Ohashi Medical Center (Takatoshi Sakurai MD); Saiseikai Yokohamashi Tobu Hospital (Mitsuhide Kitano MD); Nippon Medical School Musashikosugi Hospital (Kiyoshi Matsuda MD); Tokyo Rosai Hospital (Kotaro Tanaka MD); Toho University Omori Medical Center (Katsunori Yoshihara MD); Hiratsuka City Hospital (Kikuo Yoh MD); Yokosuka Kyosai Hospital (Junichi Suzuki MD); Saiseikai Yokohamashi Nambu Hospital (Hiroshi Toyoda MD); Nippon Medical School Chiba Hokusoh Hospital (Kunihiro Mashiko MD); Tokyo Metropolitan Children's Medical Centre (Naoki Shimizu MD); National Medical Center for Children and Mothers (Takashi Muguruma MD); Chiba Aoba Municipal Hospital (Tadanaga Shimada MD); Kuki General Hospital (Yoshiro Kobe MD); Matsudo City Hospital (Tomohisa Shoko MD); Japanese Red Cross Narita Hospital (Kazuya Nakanishi MD); Tokyo Bay Urayasu/Ichikawa Medical Center (Takashi Shiga MD); NTT Medical Center Tokyo (Takefumi Yamamoto MD); Tokyo Saiseikai Central Hospital (Kazuhiko Sekine MD); Fuji Heavy Industries Health Insurance Society OTA Memorial Hospital (Shinichi Izuka MD) (http://www.jaamkanto.jp/sos_kanto/sos_kanto2012_contributors.html).
Acknowledgments
This study was supported by the Japanese Association for Acute Medicine of Kanto. We also thank Ms. Mai Matsumoto and the secretariat of the Japanese Association for Acute Medicine of Kanto for their help in collecting the data and coordinating our project. We are proud of all the bystanders who undertook basic resuscitation in the cases described in this study and all of the firefighters, EMS, nurses, physicians, and other healthcare professionals in the Kanto region.
Name of Grant: none.
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