국제재난구조복지회

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제목	부록 - 2015 한국신폐소생술 가이드라인 영문
작성일자	2016-03-23
2015 Korean Guidelines for Cardiopulmonary Resuscitation 2016. 2 Korea Centers for Disease Control and Prevention Korean Association of Cardiopulmonary Resuscitation 2 Steering Committee for Development of 2015 Korean Guidelines for Cardiopulmonary Resuscitation Sung Oh Hwang, Chairman Department of Emergency Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea Sung Phil Chung, Department of Emergency Medicine, Yonsei University College of Medicine, Seoul, Korea Keun Jeong Song, Department of Emergency Medicine, Sungkyunkwan University College of Medicine, Seoul, Korea Hyun Kim, Department of Emergency Medicine, Yonsei University College of Medicine, Seoul, Korea Tae Ho Rho, Department of Internal Medicine, Catholic University College of Medicine, Seoul, Korea Kyu Nam Park, Department of Emergency Medicine, Catholic University College of Medicine, Seoul, Korea Young-Min Kim, Department of Emergency Medicine, Catholic University College of Medicine, Seoul, Korea June Dong Park, Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea Ai-Rhan Ellen Kim, Department of Pediatrics, Ulsan University College of Medicine, Seoul, Korea Hyuk Jun Yang, Department of Emergency Medicine, Gachon University College of Medicine, Incheon, Korea 3 Authors Part 1. The Update Process and Highlights of the 2015 Korean Guidelines for Cardiopulmonary Resuscitation Sung Oh Hwang1, Sung Phil Chung2, Keun Jeong Song3, Hyun Kim1, Tae Ho Rho4, Kyu Nam Park5, Young- Min Kim5, June Dong Park6, Ai-Rhan Ellen Kim7, Hyuk Jun Yang8 1Department of Emergency Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea, 2Department of Emergency Medicine, Yonsei Universtiy College of Medicine, Seoul, Korea, 3Department of Emergency Medicine, Sungkyunkwan University College of Medicine, Seoul, Korea, 4Department of Internal Medicine, Catholic University College of Medicine, Seoul, Korea, 5Department of Emergency Medicine, Catholic University College of Medicine, Seoul, Korea, 6Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea, 7Department of Pediatrics, Ulsan University College of Medicine, Seoul, Korea, 8Department of Emergency Medicine, Gachon University College of Medicine, Incheon, Korea Part 2. Adult Basic Life Support Keun Jeong Song1, Jae-Bum Kim2, Jinhee Kim3, Chanwoong Kim4, Sun Young Park5, Chang Hee Lee6, Yong Soo Jang7, Gyu Chong Cho8, Youngsuk Cho8, Sung Phil Chung9, Sung Oh Hwang10 1Department of Emergency Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea, 2Department of Thoracic & Cardiovascular surgery, Keimyung University School of Medicine, Daegu, Korea, 3Department of Anesthesiology, Seoul National University Bundang Hospital, Seongnam, Korea, 4Department of Emergency Medicine, College of Medicine ChungAng University, Seoul, Korea, 5Department of Nursing Science, Baekseok University, Seoul, Korea, 6Department of Emergency Medical Service, Namseoul University, Seoul, Korea, 7Department of Emergency Medicine, Hallym University Kangnam Sacred Heart Hospital, Seoul, Korea, 8Department of Emergency Medicine, Hallym University, Kangdong Sacred Heart Hospital, Seoul, Korea, 9Department of Emergency Medicine, Yonsei University College of Medicine, Wonju, Korea, 10Department of Emergency Medicine, Yonsei University Wonju College of Medicine, Seoul, Korea 4 Part 3. Advanced Life Support Mi Jin Lee1, Tai Ho Rho2, Hyun Kim3, Gu Hyun Kang4, June Soo Kim5, Sang Gyun Rho6, Hyun Kyung Park7, Dong Jin Oh8, Seil Oh9, Jin Wi10, Sangmo Je11, Sung Phil Chung12, Sung Oh Hwang3 1Department of Emergency Medicine, Kyungpook National University, College of Medicine, Daegu, Korea, 2Department of Internal Medicine, Catholic University, College of Medicine, Seoul, Korea, 3Department of Emergency Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea, 4Department of Emergency Medicine, Hallym University, College of Medicine, Seoul, Korea, 5Department of Internal Medicine, Sungkyunkwan University School of Medicine, Seoul, Korea, 6Department of Emergency Medical Services, Sunmoon University, Asan, Korea, 7Department of Emergency Medicine, Kyunghee University College of Medicine, Seoul, Korea, 8Department of Internal Medicine, Hallym University College of Medicine, Seoul, Korea, 9Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea, 10Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea, 11Department of Pediatrics, Cha University, College of Medicine, Seoul, Korea, 12Department of Emergency Medicine, Yonsei University College of Medicine, Seoul, Korea Part 4. Post-Cardiac Arrest Care Young-Min Kim1, Kyu Nam Park1, Seung Pill Choi1, Byung Kook Lee2, Kyungil Park3, Jeongmin Kim4, Ji Hoon Kim1, Sung Phil Chung5, Sung Oh Hwang6 1Department of Emergency Medicine, The Catholic University of Korea College of Medicine, Seoul, Korea, 2Department of Emergency Medicine, Chonnam National University Medical School, Kwangju, Korea, 3Department of Internal Medicine, Dong-A University College of Medicine, Busan Korea, 4Department of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, Seoul, Korea, 5Department of Emergency Medicine, Yonsei University College of Medicine, Seoul, Korea, 6Department of Emergency Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea Part 5. Pediatric Basic Life Support Ji Sook Lee1, Ji Yun Ahn2, Do Kyun Kim3, Yoon Hee Kim4, Bongjin Lee5, Won Kyoung Jhang6, Gi Beom Kim5, 5 Jin-Tae Kim7, June Huh8, June Dong Park5, Sung Phil Chung9, Sung Oh Hwang10 1Department of Emergency Medicine, Ajou University College of Medicine, Suwon, Korea, 2Department of Emergency Medicine, Hallym University College of Medicine, Seoul, Korea, 3Department of Emergency Medicine, Seoul National University College of Medicine, Seoul, Korea, 4Department of Pediatrics, Yonsei University College of Medicine, Seoul, Korea, 5Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea, 6Department of Pediatrics, Ulsan University College of Medicine, Seoul, Korea, 7Department of Anesthesiology and Pain Medicine, Seoul National University College of Medicine, Seoul, Korea, 8Department of Pediatrics, Sungkyunkwan University School of Medicine, Seoul, Korea, 9Department of Emergency Medicine, Yonsei University College of Medicine, Seoul, Korea, 10Department of Emergency Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea Part 6. Pediatric Advanced Life Support Do Kyun Kim1, Won Kyoung Jhang2, Ji Yun Ahn3, Ji Sook Lee4, Yoon Hee Kim5, Bongjin Lee6, Gi Beom Kim6 Jin-Tae Kim7, June Huh8, June Dong Park6, Sung Phil Chung9, Sung Oh Hwang10 1Department of Emergency Medicine, Seoul National University College of Medicine, Seoul, Korea, 2Department of Pediatrics, Ulsan University College of Medicine, Seoul, Korea, 3Department of Emergency Medicine, Hallym University College of Medicine, Seoul, Korea, 4Department of Emergency Medicine, Ajou University College of Medicine, Suwon, Korea, 5Department of Pediatrics, Yonsei University College of Medicine, Seoul, Korea, 6Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea, 7Department of Anesthesiology and Pain Medicine, Seoul National University College of Medicine, Seoul, Korea, 8Department of Pediatrics, Sungkyunkwan University School of Medicine, Seoul, Korea, 9Department of Emergency Medicine, Yonsei University College of Medicine, Seoul, Korea, 10Department of Emergency Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea Part 7. Neonatal Resuscitation Ai-Rhan Ellen Kim1, Han Suk Kim2, Su Jin Cho3, Yong Sung Choi4, Eun Sun Kim5, Hye Won Park6, Yong Hoon Cheon7, Moon Sung Park8, Yoon Sil Chang9, Young Han Kim10, Dong Yeon Kim11 , Hee Jo Yoon12, Yeon 6 Hee Kim13, Sung Phil Chung14, Sung Oh Hwang15 1Department of Pediatrics, University of Ulsan College of Medicine, Seoul, Korea, 2Department of Pediatrics, Seoul National University College of Medicine, Seoul, Korea, 3Department of Pediatrics, Ewha Womans University School of Medicine, Seoul, Korea, 4Department of Pediatrics, Kyung Hee University College of Medicine, Seoul, Korea, 5Department of Pediatrics, Kangwon National University College of Medicine, Chunchun, Korea, 6Department of Pediatrics, Konkuk University School of Medicine, Seoul, Korea, 7Department of Pediatrics, Inha University College of Medicine, Incheon, Korea, 8Department of Pediatrics, Ajou University College of Medicine, Suwon, Korea, 9Department of Pediatrics, Sungkyungkwan University School of Medicine, Seoul, Korea, 10Department of Obstetrics and Gynecology, Yonsei University of College of Medicine, Seoul, Korea, 11Department of Neonatal Intensive Care Unit, Catholic University of Korea Seoul St.Mary's Hospital, Seoul, Korea, 12Department of Anesthesiology and Pain Medicine, Dankook University College of Medicine, Cheonnan, Korea, 13Department of Obstetrics and Gynecology, Catholic University of Korea College of Medicine, Seoul, Korea, 14Department of Emergency Medicine, Yonsei Universtiy College of Medicine, Seoul, Korea, 15Department of Emergency Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea Part 8. Guideline for Cardiopulmonary Resuscitation Education Hyuk Jun Yang1, Gi Woon Kim2, Gyu Chong Cho3, Yang Ju Tak4, Sung Phil Chung5, Sung Oh Hwang6 1Department of Emergency Medicine, Gachon University College of Medicine, Incheon, Korea, 2Department of Emergency Medicine, Ajou University College of Medicine, Suwon, Korea, 3Department of Emergency Medicine, Hallym University College of Medicine, Seoul, Korea, 4Division of Emergency Rescue, Korea National University of Transportation College of Public Health and Life Science, Chungju, Korea, 5Department of Emergency Medicine, Yonsei University College of Medicine, Seoul, Korea, 6Department of Emergency Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea 7 Collaborators Basic Life Support: Chang Je Park, SMG-SNU Boramae Medical Center, Seoul, Korea Dae Jong Choi, Korean Red Cross, Seoul, Korea Dong Won Kim, Hallym University, Chuncheon, Korea Hee Jeong Kim, Baekseok University, Cheonan, Korea Hyun Jung Kim, Daewon University College, Jecheon, Korea Jin Hyuck Lee, Hallym University, Seoul, Korea Jin Uk Kim, Kyungdong University, Wonju, Korea Jin Woo Kim, Daejeon Health Sciences College, Daejeon, Korea Kang Nim Kim, Hallym University Kangdong Sacred Heart Hospital, Seoul, Korea Myung Lyeol Lee, Daewon University College, Jecheon, Korea Nam Sik Yoon, Chonnam National University, Gwangju, Korea Sang Wook Park, Chonnam National University Hospital, Gwangju, Korea So Hyeon Song, Daegu Health College, Daegu, Korea Su Youn Kim, Gangdong University, Icheon, Korea Advanced Life Support: Eun Jung Park, Ajou University, Suwon, Korea 8 Hyo Eun Park, Seoul National University, Seoul, Korea Jeong Hun Lee, Dongguk University, Seoul, Korea Je Sung You, Yonsei University, Seoul, Korea Jung Ho Shin, Armed Forces Capital Hospital, Seongnam, Korea Kyung Woon Jeung, Chonnam National University, Gwangju, Korea Kyu Seok Kim, Seoul National University, Seoul, Korea Sang Jin Han, Hallym University, Seoul, Korea Seog Beom Oh, Dankook University, Cheonan, Korea Seokran Yeom, Busan National University, Busan, Korea Seung Min Park, Hallym University, Pyungchon, Korea Sung Won Jang, Catholic University, Seoul, Korea Tae Yong Shin, Bundang Jesaeng General Hospital, Seongnam, Korea Young Hoon Yoon, Korea University, Seoul, Korea Post-Cardiac Arrest Care: Kyung Su Kim, Seoul National University Hospital, Seoul, Korea Won Young Kim, Ulsan University Asan Medical Center, Seoul, Korea Jin Joo Kim, Gachon University Gil Medical Center, Incheon, Korea Min Seob Sim, Sungkyunkwan University Samsung Medical Center, Seoul, Korea 9 Yeon Ho You, Chungnam National University Hospital, Kwangju, Korea Seung Joon Lee, Myongji Hospital, Seoul, Korea Young Hwan Lee, Hallym University Sacred Heart Hospital, Seoul, Korea Joo Young Lee, The Catholic University of Korea Seoul St. Mary's Hospital, Seoul, Korea Kyung Woon Jeung, Chonnam National University Hospital, Kwangju, Korea Moon Gu Han, Seoul National University Bundang Hospital, Seongnam, Korea Chul Han, Ewha University Hospital, Seoul, Korea Education: Chang Hee Lee, Namseoul university, Cheonan, Korea Dai Hai Choi, Dongguk University, Gyeongju, Korea Eun Young Park, Korean Red Cross, Seoul, Korea Gu Hyun Kang, Hallym University, Seoul, Korea InCheol Park, Yonsei University, Seoul, Korea Ji Sook Lee, Ajou University, Suwon, Korea Jong Hwan Shin, Seoul National University, Seou, Korea Jeong-Min Ryu, University of Ulsan, Seoul, Korea Kyung-Kuk Hwang, Chungbuk National University, Cheongju, Korea Sang Hoon Na, Seoul National University, Seoul, Korea Sangmo Je, Cha university, Pocheon, Korea 10 Seung Min Park, Hallym University, Pyungchon, Korea Youngsuk Cho, Hallym University, Seoul, Korea Yun Hee Oh, Asan Medical Center, Seoul, Korea Acknowledgement We thank Eun-Ju Park and Mi-Ae Shin from the Office of Korean Association of Cardiopulmonary Resuscitation for their administrative support to this work. Conflict of Interest All authors of the 2015 Korean Guidelines have documented and signed their declaration of COI. Reported COI are listed on Appendix. 11 Part 1. The Update Process and Highlights of the 2015 Korean Guidelines for Cardiopulmonary Resuscitation The background and update process of the Guidelines for Cardiopulmonary Resuscitation 1. The background of the Guidelines for Cardiopulmonary Resuscitation Cardiac arrest can occur inside medical institutions (in-hospital) and outside of medical institutions (out-ofhospital), such as in homes or public places. The incidence of cardiac arrest varies according to ethnicity, country, and region, although it is known to be 24–186 per 100,000 population.1 In South Korea, an annual survey was started in 2006 to determine the incidence of cardiac arrest, and this survey revealed that the incidence increased annually from 37.5 per 100,000 population in 2006 to 46.8 per 100,000 population in 2010.2 The survival rate for out-of-hospital cardiac arrest was 3.0% between 2006 and 2010 in South Korea, and only 0.9% of cardiac arrest cases experienced good neurologic recovery.3 The survival rate for out-of-hospital cardiac arrest has subsequently increased to approximately 5% in South Korea, although this rate is still lower than those in the US, Europe, and Japan.4-6 The prevention of cardiac arrest is the most important factor for increasing this survival rate. Furthermore, bystanders should be able to recognize the onset of cardiac arrest, initiate cardiopulmonary resuscitation (CPR), and use an automated external defibrillator. Moreover, the emergency medical system should provide a rapid response, advanced care, and efficiently facilitate in-hospital treatment for cases of cardiac arrest. Because CPR guidelines apply to the general public and healthcare providers, they should comply with each country’s ethnicity, culture, laws, and medical environment. Thus, each country develops CPR guidelines based on the latest scientific knowledge, and provides these guidelines to healthcare providers and the general public to improve survival rates among patients with cardiac arrest. In 1966, the American Heart Association and the American Academy of Science developed the first CPR guidelines, which have periodically been updated based on the available data in the related areas7.-10 In 1993, the American Heart Association and European Resuscitation Council played a pivotal role in organizing the International Liaison Committee on Resuscitation (ILCOR) to create internationally standardized CPR guidelines. The ILCOR applies newly scientific evidence to 12 the existing CPR guidelines at 5-year intervals, and the results are published as the International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations.11-13 This consensus document contains guidelines that are related to CPR, basic life support (BLS), advance life support (ALS), pediatric BLS, pediatric ALS, neonatal resuscitation (NR), education and implementation, acute coronary syndrome, and first aid.14 Therefore, when individual countries update or establish their guidelines for CPR, they use the ILCOR guidelines as a scientific basis, while also considering the country’s specific medical, legal, and cultural characteristics. The Korean Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care were established in 2006 by the Korean Association of Cardiopulmonary Resuscitation, which is operated by participating academic societies and social organizations that have an interest in CPR. The Korean Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care were updated based on emerging scientific evidence in 2011, and have been used since that time. The ILCOR announced new Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science in October 2015, which led to the updating of the 2011 Korean Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.14 2. The development scope and process for updating the Korean Guidelines for Cardiopulmonary Resuscitation The process for updating the 2011 Korean Guidelines for Cardiopulmonary Resuscitation focused issues that are directly related to cardiac arrest care. Similar to the 2011 ILCOR guidelines, the 2015 ILCOR guidelines addressed CPR, BLS, ALS, pediatric life support (PLS), NR, and education and implementation. However, the guidelines for post-cardiac arrest care, which have contributed to an increased survival rate based on recent scientific evidence, were developed separately from the guidelines for ALS. The Guidelines for Cardiopulmonary Resuscitation cover various disciplines, and required experts from all CPR-related academic societies to help develop the guidelines. Thus, the Korean Association of Cardiopulmonary Resuscitation requested the participation of expert members from the Korean Society of Emergency Medicine, the Korean Society of Cardiology, the Korean Society of Pediatrics, the Korean Society 13 of Neonatology, the Korean Society of Anesthesiologists, the Korean Neurological Association, the Korean Society of Perinatology, the Korean Nurses Association, the Korean Society of Emergency Medical Technicians, and the Korea National Red Cross. The development scope for the new Guidelines for Cardiopulmonary Resuscitation was defined using six specialties (BLS, ALS, PLS, NR, post-cardiac arrest care, and education), and expert committees were established for each specialty. These committees consisted of 1 chairperson or 2 co-chairs and 6–10 expert members that were recommend by each academic society. A steering committee, which consisted of a principal researcher and the expert committee chairs, was also established to adjust and coordinate the entire development process. Moreover, to manage any perceived conflict of interest and perform a detailed review of the evidence, an evidence review committee was formed from 119 experts (10–25 experts per speciality) who were selected by the committee chairpersons. Each expert committee selected items that required updating from the 2011 Korean Guidelines for Cardiopulmonary Resuscitation, and also identified updated items that were released by the ILCOR. These update items were classified into two types according to the review method: adaptation or hybrid updating. Items that were developed and reviewed by the ILCOR were reviewed as adaptation items. The hybrid updating items addressed topics that were described in the Korean literature or other relevant articles. Both sets of items were evaluated by the evidence review committee, who invited input from evidence review methodology experts during an educational seminar. These evidence review methodology experts provided instructions to the evidence review experts regarding the guideline update methodologies, which include the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) method; adaptation methodology; and clinical practice guideline development methodologies. The expert committees then held expert workshops to discuss the primary review results for each update item. The updates that were reviewed by the expert committees were further discussed at a consensus conference that was attended by all participating experts. The updated guidelines were developed at the consensus conference after being presented and discussed in an open forum that anyone could attend. Each expert committee created a writing committee to write the guidelines based on these discussions (Figure 1-1). 14 Figure 1-1. A developmental process of the Korean guidelines 2015 for cardiopulmonary resuscitation and emergency cardiac care. BLS: basic life support, ALS: advanced life support, PCC: post-cardiac arrest care, PLS: pediatric life support, NR: neonatal resuscitation, EI: education, implementation, ILCOR: International Liaison Committee on Resuscitation, PICO: Population, Intervention, Comparator, Outcome, AGREE: Appraisal of Guidelines for Research and Evaluation 3. Guidelines-related literature review methods The literature reviewers were recommended by the related academic societies or expert committee chairperson, and all of these reviewers completed declarations regarding any potential conflict of interest that might be related to the review, such as employment, consultation, ownership of shares, research grants, and 15 rewards. Based on feedback from the expert committee chairpersons, the Guideline Development Committee extracted 126 items (BLS: 24 items, ALS: 24 items, post-cardiac arrest care: 16 items, PLS: 21 items, NR: 25 items, education: 16 items) that have a high clinical importance and are relevant to the Korean CPR guidelines; these items are among the population, intervention, comparator, and outcome (PICO) items that were reviewed until January 2015 by ILCOR.15-19 One review owner and 1–2 other reviewers were assigned to each of the extracted PICO items, and these reviewers applied the GRADE method that was used to develop the 2015 ILCOR Guidelines for Cardiopulmonary Resuscitation.20 Only clinical research papers were considered in the literature review, and non-clinical research papers (e.g., animal studies or simulation studies) were not included. The individual expert committees evaluated the identified papers for relevance and applicability to the Korea population. New international and domestic papers that were published after January 2015 (after the ILCOR review was terminated) were also considered in the evidence review process. The reviewers submitted a draft of the Korean evidence summary and recommendations (or the Korean CPR clinical practice guidelines) to their specific expert committee, and these drafts contained the ILCOR’s evidence summary and recommendations, the reviewers’ comments, any update recommendations and justifications, domestic recommendations, and the related references. The submitted contents were reviewed by each expert committee, and then a guideline development committee workshop was organized to revise the contents based on the discussions and consensus from all committee members and reviewers who were in attendance. Three experts assessed the acceptability of the 2015 ILCOR guidelines as source guidelines, using version II of the Appraisal of Guidelines for Research & Evaluation tool.21 4. Suggestions for the recommendations grading The update recommendations for the Korean CPR clinical practice guidelines was classified into four categories, based on directivity (for or against an action) and strength (strong and weak recommendations), as recommended by the GRADE method.20 To determine the recommendation grading, the following factors were considered. First, strong recommendations were based on items with a high level of evidence, as determined according to the GRADE method for each item; the overall evidence level for each item was defined as the lowest evidence level among the key outcome variables. Second, strong recommendations were based on items 16 with a large difference between the desirable and undesirable effects of each item. Third, weak recommendations were based on low levels of reliability in an individual patient’s values and preferences. Fourth, weak recommendations were based on a greater requirement for medical resources. During the process of writing the updates, strong recommendations were indicated using the phrases “recommend” or “should do”, and weak recommendations were indicated using the phrases “suggest” or “can do”. Highlights of the 2015 Korean Guidelines for Cardiopulmonary Resuscitation The major updates of the 2015 Guidelines for Cardiopulmonary Resuscitation included: 1) a new concept regarding the Chain of Survival (introducing the importance of prevention and early detection of cardiac arrest), 2) the importance of identifying cardiac arrest during the treatment of out-of-hospital cardiac arrest and the role of emergency medical dispatchers in the CPR process, 3) chest compression-only CPR for lay rescuers, 4) an adjustment of the chest compression methods, 5) the usefulness of end-tidal carbon dioxide measurement during ALS, 6) target temperature management and coronary angiography during the process of post-cardiac arrest care, and 7) recommendations regarding mechanical and extracorporeal CPR. 1. The importance of prevention and early detection of cardiac arrest In the 2015 Korean Guidelines for Cardiopulmonary Resuscitation, the Chain of Survival includes five links: prevention and early detection of cardiac arrest, early access, early CPR, early defibrillation, and effective ALS and post-cardiac arrest care. The first link is prevention and early detection of cardiac arrest, which is newly introduced in the 2015 guidelines. This is because the survival rate is low after cardiac arrest, even if CPR is performed, and preventing the occurrence of cardiac arrest is the most effective method to reduce the number of cardiac arrest-related deaths among adults and children. However, efforts to reduce the risk of cardiovascular disease at the individual and national levels are needed to reduce the occurrence of out-of-hospital cardiac arrests. Therefore, public relations activities and public education should be used to enhance public awareness regarding the association between cardiovascular disease and cardiac arrest, and to encourage individuals to reduce their risk of cardiovascular disease. In addition, bystander response to cardiac arrest can be improved using public education regarding the premonitory symptoms of cardiac arrest, how to recognize cardiac arrest, and what to do when cardiac arrest occurs. 17 The occurrence of in-hospital cardiac arrests can be reduced by identifying patients who have a high risk of cardiac arrest, and by rapidly responding to cases of cardiac arrest.22 Therefore, medical institutions with trained medical personnel can reduce the occurrence of in-hospital cardiac arrests by maintaining rapid response or medical emergency teams. Furthermore, cardiac arrest in children is often caused by an accident or injury, and the prevention of accidents or injuries can reduce the number of cardiac arrest-related deaths among children. 2. The important role of emergency medical dispatchers In the 2015 guidelines, emphasis was placed on the role of emergency medical dispatchers in helping lay rescuers identify cardiac arrest and begin CPR. This is because most cases of cardiac arrest are witnessed by lay individuals, who are typically not trained to manage cardiac arrest and may require time and instruction to identify cardiac arrest and perform CPR. In this context, emergency medical dispatchers can provide telephone guidance to help lay rescuers identify cardiac arrest and perform CPR. This technique is associated with a higher probability of the lay rescuer initiating CPR and shortens the time to CPR initiation.23, 24 Therefore, medical service dispatchers should be trained to guide bystanders in the identification of cardiac arrest and performance of CPR. 3. Chest compression-only CPR recommended for lay rescuers Chest compression-only CPR refers chest compressions without rescue breathing. At the beginning of cardiac arrest, there is no difference in the survival rates for chest compression-only CPR or conventional CPR (rescue breathing and chest compressions), and performing only chest compressions improves the survival rate compared to that for when CPR is not performed.25-27 Even if they have received CPR training, many lay persons do not perform adequate mouth-to-mouth rescue breathing, and they may not attempt CPR due to their reluctance to perform rescue breathing. Therefore, the 2015 guidelines recommend chest compression-only CPR for lay rescuers, although conventional CPR is recommended for rescuers who are able to perform rescue breathing and intend to do so. Furthermore, chest compression-only CPR is recommended when emergency medical dispatchers guide lay rescuers in the performance of CPR. 4. Adjustment of chest compression depth and rate The 2015 guidelines recommend high-quality CPR that provides adequate chest compression depth and rate, 18 sufficient relaxation, and minimal interruptions. The recommendations regarding chest compression depth and rate were updated in the new guidelines based on the scientific evidence and expert opinion.28, 29 The 2011 guidelines recommend compression depths of 4 cm for infants, 5 cm for children, and ≥5 cm for adults (up to 6 cm). In contrast, the 2015 guidelines recommend compression depths of 4 cm for infants, 4–5 cm for children, and approximately 5 cm for adults (to a maximum of 6 cm.). Furthermore, the 2011 guidelines recommend a chest compression rate of ≥100 times per minute (up to 120 times per minute) for adults and children, whereas the 2015 guidelines recommend a rate of 100–120 times per minute for adults and children. However, the recommendations regarding the location of chest compression, chest compression to ventilation ratio, sufficient relaxation after chest compression, and minimizing interruptions remain the same as those in the 2011 guidelines 5. Emphasizing the usefulness of end-tidal carbon dioxide measurement during ALS There are few methods for evaluating a patient’s hemodynamic status during CPR or the effectiveness of the CPR. However, the partial pressure of end-tidal carbon dioxide (the partial pressure of carbon dioxide in exhaled air) changes in response to the proportion of lung perfusion during CPR. Therefore, this pressure can be used to assess the adequacy of chest compressions and the possibility of the return of spontaneous circulation (ROSC).30, 31 In addition, the partial pressure of end-tidal carbon dioxide can be used to check whether an intubated tube was correctly placed after endotracheal intubation.32 Therefore, the 2015 guidelines recommend using the partial pressure of end-tidal carbon oxide to assess the effectiveness of CPR, estimate the possibility of ROSC, and locate the endotracheal tube. 6. Recommendations regarding target temperature management and coronary angiography during postcardiac arrest care Updates were made to the items for hypothermia and coronary angiography, which are the main treatments during post-cardiac arrest care. The 2011 guidelines recommended target temperature management at 32–34°C, whereas the 2015 guidelines were updated to recommend a target of 32–36°C for ≥24 h among adults who are unresponsive after ROSC, based on recent evidence regarding core temperature control.33-35 The 2015 guidelines also recommend considering temperature management during post-cardiac care for pediatric patients who are 19 unresponsive after ROSC due to cardiac arrest, and especially to prevent fever among children. Coronary angiography is performed to identify coronary artery disease as the main cause of cardiac arrest, and appropriate coronary interventions are important treatments that can increase the post-cardiac arrest survival rate.36, 37 The 2015 guidelines recommend performing emergency coronary angiography if ST elevation is observed on an electrocardiogram, regardless of the patient’s state of consciousness after ROSC, and suggest considering emergency coronary angiography in cases that may be caused by acute coronary syndrome, even if ST elevation is not observed. In addition, the 2015 guidelines recommend that patients who achieve ROSC after cardiac arrest be treated at hospitals where target temperature management and coronary interventions are available 24 h/day (i.e., a post-cardiac arrest care center). 7. Recommendations regarding automatic mechanical CPR devices and extracorporeal CPR Automatic mechanical CPR devices eliminate the need for manual chest compressions, although the survival rates were not significantly different when studies compared automatic mechanical CPR devices and manual CPR.38-40 Based on these results, the 2015 guidelines do not recommend the use of automatic mechanical CPR devices as a routine alternative to the current CPR protocol. However, automatic mechanical CPR devices may be useful while transferring patients in an ambulance or helicopter, or while performing angiography or extracorporeal CPR. Extracorporeal CPR maintains artificial circulation using an extracorporeal device in patients with cardiac arrest who do not respond to conventional CPR, and this method can improve the survival rate when it is selectively used by trained personnel in properly equipped hospitals.41, 42 The 2015 guidelines recommend that, in hospitals with trained personnel who are capable of using extracorporeal devices, extracorporeal CPR should be considered for patients with cardiac arrest who do not achieve ROSC despite receiving conventional ALS. 20 Appendix 1. The 2015 Korean Guidelines Writing Group Disclosure of COI. Author name COI Ai-Rhan Ellen Kim Chair, Neonatal resuscitation taskforce, Korean Guidelines for CPR (2011, 2015) Chair, Neonatal resuscitation committee, Korean Association of CPR Bongjin Lee No COI reported Byung Kook Lee No COI reported Chang Hee Lee No COI reported Chanwoong Kim No COI reported Do Kyun Kim No COI reported Dong Jin Oh No COI reported Dong Yeon Kim Consultant, Elsevier nursing skills education program (2012) Eun Sun Kim No COI reported Gi Beom Kim No COI reported Gi Woon Kim No COI reported Gu Hyun Kang No COI reported Gyu Chong Cho No COI reported Han Suk Kim 2015 ILCOR evidence reviewer, Neonatal resuscitation Hee Jo Yoon No COI reported Hye Won Park No COI reported Hyuk Jun Yang 2015 ILCOR First Aid taskforce member, 2015 ILCOR question owner, Hyun Kim Co-chair, ALS taskforce, Korean Guidelines for CPR (2015) Chair, ALS committee, Korean Association of CPR Hyun Kyung Park No COI reported Jae-Bum Kim No COI reported Jeongmin Kim No COI reported Ji Hoon Kim No COI reported Ji Sook Lee No COI reported 21 Ji Yun Ahn No COI reported Jin Wi No COI reported Jinhee Kim No COI reported Jin-Tae Kim No COI reported June Dong Park Chair, PLS taskforce, Korean Guidelines for CPR (2011, 2015) Chair, PLS committee, Korean Association of CPR June Huh No COI reported June Soo Kim Chair, Publication committee, Korean Association of CPR Keun Jeong Song Chair, BLS taskforce, Korean Guidelines for CPR (2011, 2015) Chair, BLS committee, Korean Association of CPR Kyu Nam Park Co-chair, Post-cardiac arrest care taskforce, Korean Guidelines for CPR (2011, 2015) Chair, Planning and Coordinating committee, Korean Association of CPR Kyungil Park No COI reported Mi Jin Lee No COI reported Moon Sung Park No COI reported Sang Gyun Rho No COI reported Sangmo Je No COI reported Seil Oh No COI reported Seung Pill Choi No COI reported Su Jin Cho No COI reported Sun Young Park No COI reported Sung Oh Hwang Chair, Korean Guidelines for CPR (2006, 2011, 2015) General secretary, Korean Association of CPR Patent holder of an automatic CPR device No financial COI reported Sung Phil Chung ILCOR evidence reviewer, BLS (2010, 2015) Chair, Evidence Review and COI management taskforce, Korean Guidelines for CPR (2015) Tai Ho Rho Co-chair, ALS taskforce, Korean Guidelines for CPR (2015) 22 Won Kyoung Jhang No COI reported Yang Ju Tak No COI reported Yeon Hee Kim No COI reported Yong Hoon Cheon No COI reported Yong Soo Jang No COI reported Yong Sung Choi No COI reported Yoon Hee Kim No COI reported Yoon Sil Chang No COI reported Young Han Kim No COI reported Young Min Kim Co-chair, Post-cardiac arrest care taskforce, Korean Guidelines for CPR (2015) Program director of Asia TTM master class sponsored by BARD (2013, 2014) Youngsuk Cho No COI reported 23 References 1. Berdowski J, Berg RA, Tijssen JG, Koster RW. Global incidences of out-of-hospital cardiac arrest and survival rates: Systematic review of 67 prospective studies. Resuscitation 2010;81:1479-87. 2. Ro YS, Shin SD, Song KJ, et al. A trend in epidemiology and outcomes of out-of-hospital cardiac arrest by urbanization level: a nationwide observational study from 2006 to 2010 in South Korea. Resuscitation 2013;84:547-57. 3. Ro YS, Hwang SS, Shin SD, et al. Presumed Regional Incidence Rate of Out-of-Hospital Cardiac Arrest in Korea. J Korean Med Sci 2015;30:1396-404. 4. Chan PS, McNally B, Tang F, Kellermann A, Group CS. Recent trends in survival from out-of-hospital cardiac arrest in the United States. Circulation 2014;130:1876-82. 5. Stromsoe A, Svensson L, Axelsson AB, et al. Improved outcome in Sweden after out-of-hospital cardiac arrest and possible association with improvements in every link in the chain of survival. Eur Heart J 2015;36:863-71. 6. Kitamura T, Iwami T, Kawamura T, et al. Nationwide improvements in survival from out-of-hospital cardiac arrest in Japan. Circulation 2012;126:2834-43. 7. Cardiopulmonary resuscitation. JAMA 1966;198:372-9. 8. Proceedings of the 1985 National Conference on Standards and Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiac Care. July 11-13, Dallas, Texas. Circulation 1986;74:IV1-153. 9. National Conference on Cardiopulmonary R, Emergency Cardiac C. Standards and guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care (ECC). Part VIII: Medicolegal considerations and recommendations. JAMA 1986;255:2979-84. 10. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. Emergency Cardiac Care Committee and Subcommittees, American Heart Association. Part I. Introduction. JAMA 1992;268:2171-83. 11. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 3: adult basic life support. The American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Circulation 2000;102:I22-59. 12. International Liaison Committee on R. 2005 International Consensus on Cardiopulmonary Resuscitation and 24 Emergency Cardiovascular Care Science with Treatment Recommendations. Part 1: introduction. Resuscitation 2005;67:181-6. 13. Hazinski MF, Nolan JP, Billi JE, et al. Part 1: Executive summary: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation 2010;122:S250-75. 14. Hazinski MF, Nolan JP, Aickin R, et al. Part 1: Executive Summary: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation 2015;132:S2-S39. 15. Finn JC, Bhanji F, Lockey A, et al. Part 8: Education, implementation, and teams: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation 2015;95:e203-24. 16. Soar J, Callaway CW, Aibiki M, et al. Part 4: Advanced life support: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation 2015;95:e71-e120. 17. Perkins GD, Travers AH, Berg RA, et al. Part 3: Adult basic life support and automated external defibrillation: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation 2015;95:e43-69. 18. Wyllie J, Perlman JM, Kattwinkel J, et al. Part 7: Neonatal resuscitation: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation 2015;95:e169-201. 19. Maconochie IK, de Caen AR, Aickin R, et al. Part 6: Pediatric basic life support and pediatric advanced life support: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation 2015;95:e147-68. 20. Schünemann H, Bro˙zek J, Guyatt G, Oxman A. GRADE handbook; 2013. http://www.guidelinedevelopment.org/handbook (accessed December 4, 2015). 21. Brouwers MC, Kho ME, Browman GP, et al. AGREE II: advancing guideline development, reporting and evaluation in health care. CMAJ 2010;182:E839-42. 22. Maharaj R, Raffaele I, Wendon J. Rapid response systems: a systematic review and meta-analysis. Crit Care 25 2015;19:254. 23. Lewis M, Stubbs BA, Eisenberg MS. Dispatcher-assisted cardiopulmonary resuscitation: time to identify cardiac arrest and deliver chest compression instructions. Circulation 2013;128:1522-30. 24. Bohm K, Stalhandske B, Rosenqvist M, Ulfvarson J, Hollenberg J, Svensson L. Tuition of emergency medical dispatchers in the recognition of agonal respiration increases the use of telephone assisted CPR. Resuscitation 2009;80:1025-8. 25. Rea TD, Fahrenbruch C, Culley L, et al. CPR with chest compression alone or with rescue breathing. N Engl J Med 2010;363:423-33. 26. Svensson L, Bohm K, Castren M, et al. Compression-only CPR or standard CPR in out-of-hospital cardiac arrest. N Engl J Med 2010;363:434-42. 27. Iwami T, Kitamura T, Kiyohara K, Kawamura T. Dissemination of Chest Compression-Only Cardiopulmonary Resuscitation and Survival After Out-of-Hospital Cardiac Arrest. Circulation 2015;132:415- 22. 28. Stiell IG, Brown SP, Nichol G, et al. What is the optimal chest compression depth during out-of-hospital cardiac arrest resuscitation of adult patients? Circulation 2014;130:1962-70. 29. Idris AH, Guffey D, Pepe PE, et al. Chest compression rates and survival following out-of-hospital cardiac arrest. Crit Care Med 2015;43:840-8. 30. Pearce AK, Davis DP, Minokadeh A, Sell RE. Initial end-tidal carbon dioxide as a prognostic indicator for inpatient PEA arrest. Resuscitation 2015;92:77-81. 31. Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest. N Engl J Med 1997;337:301-6. 32. Silvestri S, Ralls GA, Krauss B, et al. The effectiveness of out-of-hospital use of continuous end-tidal carbon dioxide monitoring on the rate of unrecognized misplaced intubation within a regional emergency medical services system. Ann Emerg Med 2005;45:497-503. 33. Hypothermia after Cardiac Arrest Study G. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346:549-56. 34. Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557-63. 26 35. Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33 degrees C versus 36 degrees C after cardiac arrest. N Engl J Med 2013;369:2197-206. 36. Hollenbeck RD, McPherson JA, Mooney MR, et al. Early cardiac catheterization is associated with improved survival in comatose survivors of cardiac arrest without STEMI. Resuscitation 2014;85:88-95. 37. Strote JA, Maynard C, Olsufka M, et al. Comparison of role of early (less than six hours) to later (more than six hours) or no cardiac catheterization after resuscitation from out-of-hospital cardiac arrest. Am J Cardiol 2012;109:451-4. 38. Wik L, Olsen JA, Persse D, et al. Manual vs. integrated automatic load-distributing band CPR with equal survival after out of hospital cardiac arrest. The randomized CIRC trial. Resuscitation 2014;85:741-8. 39. Rubertsson S, Lindgren E, Smekal D, et al. Mechanical chest compressions and simultaneous defibrillation vs conventional cardiopulmonary resuscitation in out-of-hospital cardiac arrest: the LINC randomized trial. JAMA 2014;311:53-61. 40. Perkins GD, Lall R, Quinn T, et al. Mechanical versus manual chest compression for out-of-hospital cardiac arrest (PARAMEDIC): a pragmatic, cluster randomised controlled trial. Lancet 2015;385:947-55. 41. Sakamoto T, Morimura N, Nagao K, et al. Extracorporeal cardiopulmonary resuscitation versus conventional cardiopulmonary resuscitation in adults with out-of-hospital cardiac arrest: a prospective observational study. Resuscitation 2014;85:762-8. 42. Chen YS, Lin JW, Yu HY, et al. Cardiopulmonary resuscitation with assisted extracorporeal life-support versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an observational study and propensity analysis. Lancet 2008;372:554-61. 27 Part 2. Adult Basic Life Support Chain of Survival Chain of survival is a series of steps required to increase the survival rate of patients with cardiac arrest. To increase the survival rate of patients with cardiac arrest, chain of survival should be strengthened in a community. Chain of survival in 2015 Korean cardiopulmonary resuscitation (CPR) guidelines is composed of five chains: the prevention and immediate recognition of cardiac arrest, early access (activation of emergency medical system [EMS]), early CPR, early defibrillation, and effective advanced life support and post-cardiac arrest care (Figure 2-1). Figure 2-1. Chain of survival in 2015 Korean cardiopulmonary resuscitation guidelines. Components of chain of survival are the prevention and immediate recognition of cardiac arrest, early access, early CPR, early defibrillation, and effective advanced life support and post-cardiac arrest care. 1. The prevention and immediate recognition of cardiac arrest The new concept of preventing and immediately recognizing cardiac arrest was newly introduced in 2015 Korean CPR guidelines as the first link in the chain of survival. The development of cardiac arrest can be prevented by reducing the risk factors of cardiac and cerebrovascular diseases in adults.1 Efforts need to be made to reduce these risk factors and precipitating factors that cause cardiac arrest. Inside of a hospital, the signs and symptoms presenting prior to cardiac arrest need to be rapidly recognized and treated. The medical emergency team or rapid response team have a role in this process.2, 3 Lay people should be taught 28 about signs or symptoms of cardiac arrest, which will increase their ability to recognize cardiac arrest. 2. Early access The second link in the chain of survival is early access which includes making a phone call to the 119 EMS center and activating EMS. A bystander recognizing cardiac arrest calls the 119 emergency medical services and reports an incidence of cardiac arrest. The emergency medical dispatcher who receives the call dispatches an ambulance and emergency personnel to the scene. The emergency medical dispatcher should have an ability to instruct CPR via telephone to the bystander. 3. Early CPR Immediately after the call to 119 EMS center, a bystander should immediately start and continue CPR until emergency personnel arrive. CPR performed by a bystander increases the survival rate of the victims with cardiac arrest.4 To increase the rate of bystander CPR, schools, militaries, residential areas, work places, and public institutions need to provide education on CPR. 4. Early defibrillation Defibrillation is the most important intervention to treat ventricular fibrillation (VF). Defibrillation is more effective when it is performed early after VF develops.5 An automated external defibrillator (AED) is used for early defibrillation. If an AED is installed in public places through a public access defibrillation (PAD) program, the survival rate of patients with VF remarkably increases with early defibrillation.6 AED can be safely used by lay persons after they receives a brief instruction to use. 5. Effective advanced life support and post-cardiac arrest care Effective advanced life support (ALS) needs to be performed to restore the spontaneous circulation of patients with cardiac arrest. Integrated post-cardiac arrest care is required for patients whose spontaneous circulation has recovered from cardiac arrest. Post-cardiac arrest care is an integrated treatment process that includes general intensive care, targeted temperature management (TTM), percutaneous coronary intervention (PCI) for acute coronary syndrome, and the seizure control.7-9 Patients resuscitated from cardiac arrest need to be transported to 29 a medical center or facility where integrated post-cardiac arrest care including TTM or PCI can be performed.10 Major update of the 2015 Korean basic life support guidelines The main contents newly added or revised in the 2015 Korean basic life support (BLS) guideline are as follows. a) Cardiac arrest should be immediately evaluated by the presence of apnea or abnormal respiration. Abnormal respiration represents all forms of respiration that are not normal, such as apnea or agonal gasps.11 b) Healthcare providers also need to simultaneously check the patient’s pulse and respiration within 10 sec, and they should not delay compression to check for the absence or presence of a pulse. c) Regarding the order of CPR, chest compression needs to be performed prior to breathing. Similar to the guideline in 2011, the order of compression-airway-breathing (C-A-B sequence) needs to be maintained.11, 12 d) High quality CPR is important. It is suggested that in adult patients with cardiac arrest, the depth of compression should be approximately 5 cm, and the rate should be 100–120/min. It is recommended that the interruption of compression is minimized to less than 10 sec, and breathing should not be excessively performed. 11-18 e) Healthcare providers, including 119 emergency medical technicians (EMTs), should always perform CPR with both compression and ventilation. Adult Basic Life Support (BLS) for Lay Rescuers 2015 Korean CPR guidelines recommend compression-only CPR when a non-healthcare professional lay person rescues a victim with cardiac arrest. The steps of BLS consist of determining unresponsiveness, calling the 119 emergency dispatcher center, performing compression-only CPR, and using an AED. The sequence of adult BLS for lay persons is summarized in BLS algorithm for lay rescuers (Figure 2-2). 30 Figure 2-2. BLS algorithm for lay rescuers AED, automated external defibrillator; CPR, cardiopulmonary resuscitation 1. Check for responsiveness The first step of BLS is to check for responsiveness. The safety of the scene needs to be assessed first before approaching the collapsed person. Responsiveness can be evaluated by shouting, “Are you alright?” to the collapsed person, and by tapping his/her shoulder. 2. 119 emergency call If the collapsed person is unresponsive, a 119 emergency call should be made immediately, and an AED needs 31 to be requested. If one witnesses a collapsed person, he/she needs to request that someone call 119 by loudly asking others nearby for help. One should also call 119 if there is no one else around. When calling 119, the location of the incidence, situation of the incidence, the patient’s status, and emergency treatment that is being conducting needs to be reported.1 3. Assessing respiration (recognition of cardiac arrest) The patient’s respiration should be evaluated after checking responsiveness and making the 119 call. Patients who are unresponsive and have apnea or abnormal respiration (e.g., agonal respiration) should be determined to be in cardiac arrest. It is challenging for a lay rescuer to precisely evaluate the patient’s respiration status.19 Thus, a lay rescuer needs the help of an emergency medical dispatcher to determine the respiration status and to provide guidance on how to perform compression-only CPR.20 4. Compression-only CPR It is recommended that lay rescuers perform compression-only CPR for adult victims with cardiac arrest. The blood oxygen concentration does not rapidly decrease when cardiac arrest suddenly occurs without hypoxia such as in cases of cardiac arrest from cardiac origin.; instead, it may maintain for a few minutes at the early stage of cardiac arrest.21 Therefore, ventilation may not be necessary during the early stage of cardiac arrest. According to a series of recent clinical trials, the survival rate increases with compression-only CPR compared to no CPR.22, 23 Also, compression-only CPR has a similar survival rate compared to standard CPR that includes ventilation in patients with cardiac arrest of non-respiratory origin.24 Standard CPR is recommended if the rescuer knows how to ventilate and is willing to provide ventilation. In adult cardiac arrest, the depth of compression should be approximately 5 cm, and the rate should be maintained at 100–120/min.15, 25 The recommended position of one’s hand when performing compression is at the lower half of the sternum. If the depth of compression is greater than 6 cm, there is a possibility of increasing incidence of complications.26 32 5. AED use An AED should be used immediately when it arrives. If an AED arrives while CPR is being performed, one needs to push the power button to turn it on. After taking off the patient’s shirt, two pads need to be firmly attached to the patient’s bare chest. Chest compressions need to be stopped while the AED analyzes the cardiac rhythm of the patient with cardiac arrest. If defibrillation is required, the AED says, “need defibrillation” and charges the defibrillator by itself. If a voice or screen instruction says, “push the shock button” after charging, one must ensure that no one touches the patient for safety purposes, and then the shock button can be pushed. One must resume chest compressions immediately after defibrillation. Dispatcher-assisted CPR The emergency medical dispatcher can assist a lay rescuer to recognize cardiac arrest and instruct CPR. An emergency medical dispatcher asks the caller if the collapsed person is responsive and if his/her respiration is abnormal.27 An emergency medical dispatcher determines cardiac arrest in cases in which the collapsed person is unresponsive and has apnea or abnormal respiration. If an emergency medical dispatcher recognizes cardiac arrest, the dispatcher will provide instructions on how to perform CPR via telephone. Instruction of compression-only CPR to lay rescuers by emergency dispatchers increases bystander CPR rate and improves the survival rate of victims with cardiac arrest.27-29 If the patient with cardiac arrest is submerged or hypoxic, or the rescuer is able to perform breathing, both chest compression and breathing need to be performed. Exemption of the liability in the Korean Emergency Medical Service law There is an exemption clause in the Korean Emergency Medical Service law about liability of the rescuer who provides emergency treatment. The fifth subsection and second article of this law articulates the following: “When a person renders first aid or emergency care to an emergency patient whose life is at stake and there is no intentional or severe fault on property damage or injuries as a result of his/her acts, he/she shall not be liable for any civil damages and has no criminal liability including for the victim’s death”. 30 This law protects good Samaritans. Basic Life Support for Healthcare Providers 33 The steps of BLS for healthcare providers consist of determining unresponsiveness, calling the 119 emergency dispatcher center, checking for breathing and pulse, performing CPR, and using an AED or defibrillator. The sequence of adult BLS for healthcare providers is summarized in BLS algorithm for healthcare providers (Figure 2-3). Figure 2-3. BLS algorithm for healthcare providers AED, automated external defibrillator; CPR, cardiopulmonary resuscitation 1. Check unresponsiveness, call the 119 dispatcher center As in BLS for lay persons, the first step of BLS is to check for unresponsiveness. The safety of the scene needs to be assessed first before approaching the collapsed person. Unresponsiveness can be evaluated by shouting, 34 “Are you alright?” to the collapsed person, and by tapping his/her shoulder. 2. Assessing respiration and pulse The patient’s respiration should be evaluated after determining responsiveness and making the 119 call. Determination of the absence or presence of a pulse and respiration should be performed within 10 sec. To determine the pulse of an adult patient with cardiac arrest, the carotid artery needs to be assessed.11 3. Chest compression In adult cardiac arrest, the depth of compression should be approximately 5 cm, and the rate should be maintained at 100–120/min.15, 25 The recommended position of one’s hand when performing compression is at the lower half of the sternum. If the depth of compression is greater than 6 cm, there is a possibility of increasing complications.26 The recoil of the chest needs to be maximized after each compression.31, 32 The suggested compression-ventilation ratio is 30:2.33-35 Considering the high quality of CPR and the fatigue of a rescuer, a role of compressor needs to rotate every 2 min.11The interruption of compression should be minimized to less than 10 sec during CPR.16, 18, 36 In the case that an advanced airway is in place, it is suggested that one rescuer continues compression at a rate of 100–120/min without interruption, and the other rescuer provides respiration with a bag valve mask every 6 sec (10 breaths/min). Healthcare providers, including 119 emergency medical technicians, should always perform CPR with both compression and ventilation.11, 21, 25 4. Airway and rescue breathing When healthcare providers open the airway of patients with cardiac arrest and no evidence of injuries to the head or neck, the airway should always be maintained by using the head tilt-chin lift maneuver. If a cervical injury is suspected, the jaw thrust technique, which does not include head extension, should be used to open the airway. Mouth-to-mouth ventilation is recommended to provide rescue breathing to the patient. We recommend to 35 ventilate the patient with inspiration duration of 1 sec and with the tidal volume as the patient’s rising chest is visually identified. Provide ventilation once every 6 sec (10 breaths/min) if there are two or more healthcare providers and an advanced airway is inserted. Avoid hyperventilation during rescue breathing. The tidal volume should be maintained at 500–600 mL (6–7 mL/kg) during adult CPR.37-39 The most common cause of failure in ventilation is inappropriate opening of the airway. If the patient’s chest does not rise during the first attempt of breathing, breathing should be conducted again after properly performing the head tilt-chin lift maneuver. When respiration assistance is needed for a patient with spontaneous circulation (e.g., when a strong pulse is palpable), ventilation should be performed every 5–6 sec or 10–12/minutes. Bag mask ventilation is a method to provide positive pressure ventilation without an advanced airway. A rescuer provides about 500– 600 mL of tidal volume using an adult bag mask. This should be performed for 1 sec, and oxygen (concentration greater than 40%, minimum 10–12 L/min) should be provided if possible.40 It is most effective when two or more experienced rescuers use the bag mask. After the advanced airway is placed, chest compression should be performed at 100–120/min without interruption, and ventilation should be performed every 6 sec (10 breaths/min). Healthcare providers can choose either a bag mask or advanced airway while CPR is performed in adult patients with cardiac arrest. To provide an advanced airway, either a supraglottic airway or endotracheal tube can be placed. 5. AED use An AED should be used immediately when it arrives. If an AED arrives while CPR is being performed, one rescuers use an AED and the other continues CPR. Chest compression should not be stopped except a period for analyzing rhythm and delivering a shock. After delivering a shock, immediately restart chest compression. After every 2 min of CPR, analyze the cardiac rhythm and check the patient’s status. Advanced life support should be started if available. 36 References 1. Goyal V, Jassal DS, Dhalla NS. Pathophysiology and prevention of sudden cardiac death. Can J Physiol Pharmacol 2015: 1-8. 2. Salvatierra G, Bindler RC, Corbett C, Roll J, Daratha KB. Rapid response team implementation and inhospital mortality. Crit Care Med 2014; 42: 2001-6. 3. 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Moller Nielsen A, Rasmussen LS. Damage and depth of chest compressions. Resuscitation 2013; 84: 713-4. 27. Becker LB, Pepe PE. Ensuring the effectiveness of community-wide emergency cardiac care. Ann Emerg Med 1993; 22: 354-65. 28. Svensson L, Bohm K, Castren M, et al. Compression-only CPR or standard CPR in out-of-hospital cardiac arrest. N Engl J Med 2010; 363: 434-42. 29. Iwami T, Kitamura T, Kiyohara K, Kawamura T. Dissemination of Chest Compression-Only Cardiopulmonary Resuscitation and Survival After Out-of-Hospital Cardiac Arrest. Circulation 2015; 132: 415- 22. 30. El Hajj SC, Bordelon CJ, Glancy DL. ECG Case of the Month: Out-of-Hospital Cardiac Arrest. J La State Med Soc 2014; 166: 176-8. 39 31. Zuercher M, Hilwig RW, Ranger-Moore J, et al. Leaning during chest compressions impairs cardiac output and left ventricular myocardial blood flow in piglet cardiac arrest. Crit Care Med 2010; 38: 1141-6. 32. Yannopoulos D, McKnite S, Aufderheide TP, et al. Effects of incomplete chest wall decompression during cardiopulmonary resuscitation on coronary and cerebral perfusion pressures in a porcine model of cardiac arrest. Resuscitation 2005; 64: 363-72. 33. Gazmuri RJ, Ayoub IM, Radhakrishnan J, Motl J, Upadhyaya MP. Clinically plausible hyperventilation does not exert adverse hemodynamic effects during CPR but markedly reduces end-tidal PCO(2). Resuscitation 2012; 83: 259-64. 34. Kill C, Galbas M, Neuhaus C, et al. Chest Compression Synchronized Ventilation versus Intermitted Positive Pressure Ventilation during Cardiopulmonary Resuscitation in a Pig Model. PLoS One 2015; 10: e0127759. 35. Abella BS, Alvarado JP, Myklebust H, et al. Quality of cardiopulmonary resuscitation during in-hospital cardiac arrest. JAMA 2005; 293: 305-10. 36. Cheskes S, Schmicker RH, Verbeek PR, et al. The impact of peri-shock pause on survival from out-ofhospital shockable cardiac arrest during the Resuscitation Outcomes Consortium PRIMED trial. Resuscitation 2014; 85: 336-42. 37. Wenzel V, Keller C, Idris AH, Dorges V, Lindner KH, Brimacombe JR. Effects of smaller tidal volumes during basic life support ventilation in patients with respiratory arrest: good ventilation, less risk? Resuscitation 1999; 43: 25-9. 38. Dorges V, Ocker H, Hagelberg S, Wenzel V, Idris AH, Schmucker P. Smaller tidal volumes with room-air are not sufficient to ensure adequate oxygenation during bag-valve-mask ventilation. Resuscitation 2000; 44: 37-41. 39. Dorges V, Ocker H, Hagelberg S, Wenzel V, Schmucker P. Optimisation of tidal volumes given with selfinflatable bags without additional oxygen. Resuscitation 2000; 43: 195-9. 40 40. Kilgannon JH, Jones AE, Shapiro NI, et al. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA 2010; 303: 2165-71. 41 Part 3. Advanced Cardiac Life Support Background of 2015 Guidelines for adult Advanced Life Support The chain of survival suggested in the 2015 Korean Guidelines on Cardiopulmonary Resuscitation (CPR) consists of the five links of prevention and early detection of cardiac arrest, early access, early CPR, early defibrillation, and effective advanced life support (ALS) and post-cardiac arrest care. ALS, which constitutes the last link, should immediately follow the basic life support (BLS) if the required manpower, equipment, and drugs are available. ALS includes the following elements: quick recognition of cardiac arrest and activation of the resuscitation team; immediate CPR, manual defibrillation, and pharmacological therapy; and advanced airway management and monitoring of physiological parameters.1 Comprehensive post-cardiac arrest care, which begins immediately after recovery of spontaneous circulation, is also included in ALS. Improvements in the survival and neurologic outcomes in patients with cardiac arrest can be expected only when BLS and ALS are provided in combination. In case of in-hospital cardiac arrest, effective BLS begins with the first responder quickly confirming cardiac arrest, immediately calling for help, asking for manual defibrillator while calling the resuscitation team in the hospital, and conducting a high-quality CPR. The most important principle in cardiac arrest treatment through ALS is that it should be based on effective BLS. When ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) occurs, the survival rate can be increased with immediate CPR and early defibrillation conducted by the witness. Advanced airway management, mechanical chest compression devices, and extracorporeal circulation devices increase the short-term survival rate including the return of spontaneous circulation (ROSC) and survival admission.2-7 However, the evidence supporting that these improve the survival or neurologic outcomes at hospital discharge is still insufficient. Long-term survival of patients who recover their spontaneous circulation can be improved when combined post-cardiac arrest treatment, which includes targeted temperature management (TTM) and percutaneous coronary intervention (PCI), is provided in association with high-quality BLS and effective ALS.8-15 The incidence rate of inhospital cardiac arrest can be decreased by early recognition of patients with deteriorating condition indicating an impending cardiac arrest and responding immediately.16 The major issues of ALS described in the 2015 Korean CPR Guidelines maintained the basic principles 42 suggested in the 2011 Korean CPR Guidelines. The 2015 Guidelines continue to emphasize on the importance of immediate and effective CPR (chest compression with adequate depth and rate, sufficient relaxation, minimal interruption of chest compression, and prevention of hyperventilation) in patients who experience cardiac arrest. 17-21 During CPR, the ALS provider uses available monitoring devices, such as end-tidal carbon dioxide (ETCO2) monitoring devices and pulse oximeter, supplies oxygen via advanced airway, and conducts manual defibrillation. Furthermore, during ALS, the provider finds the reversible causes of cardiac arrest and corrects them if possible. As ways of advanced airway management, the use of supraglottic airway devices (e.g. laryngeal mask airway, laryngeal tube, i-gel) is recommended in addition to endotracheal intubation.22-24 However, the Guideline emphasizes that chest compression should not be delayed due to advanced airway management conducted during CPR. Highlights of 2015 Guidelines for adult Advanced Life Support The key issues and the major highlights of the 2015 Korean Guidelines for ALS include the following. Monitoring physiologic parameters during CPR provides meaningful information about the patient’s condition and response to CPR. These parameters can be monitored continuously, without interrupting chest compression. The use of quantitative waveform capnography for monitoring of the partial pressure of ETCO2 is recommended after advanced airway management. Capnography is useful for evaluating the effectiveness of chest compression and the possibility of the return of spontaneous circulation (ROSC) during CPR.25, 26 Low ETCO2 in intubated patients after 20 minutes of CPR is associated with poor chances for ROSC and survival.26, 27 When quantitative capnography is used after endotracheal intubation, the healthcare providers can confirm an intratracheal placement of endotracheal tube.28, 29 With regard to vasopressors for cardiac arrest treatment, the combination of vasopressin and epinephrine offers no advantage over the standard-dose epinephrine. Vasopressin has been removed from the adult out-of-hospital cardiac arrest algorithm. However, as per the 2015 Korean CPR Guidelines for ALS, vasopressin may provide some benefit when bundled with epinephrine and steroids in treating in-hospital cardiac arrest.30, 31 43 Although mechanical chest compression devices have been developed and are currently being used in cardiac arrest patients, the use of such devices as a routine alternative to the conventional CPR is not recommended. Manual chest compression remains the standard care for cardiac arrest; however, in certain circumstances (e.g. in case of limited manpower or prolonged CPR, when in a moving ambulance or helicopter, in the angiography room, or during preparation of extracorporeal CPR [ECPR]), the use of mechanical chest compression devices can be considered as a reasonable alternative to high-quality chest compression.5, 32, 33 ECPR is a complex intervention that requires a highly trained team, specialized equipment, and multidisciplinary support. Only for selected patients who have a cardiac arrest and for whom the suspected etiology of cardiac arrest is potentially reversible, ECPR may be considered an alternative to conventional CPR.6, 7 Cardiac arrest algorithm in adult Because the necessity of defibrillation and the drugs administered for treatment of cardiac arrest differ depending on electrocardiography (ECG) rhythms, understanding of the entire algorithm and initial ECG rhythms is essential for effective ALS. Cardiac rhythms during cardiac arrest include shockable rhythms (VF and pulseless VT) and non-shockable rhythms (asystole and pulseless electrical activity [PEA]). BLS and early defibrillation, rather than advanced airway management or drug administration, are the most important and preferentially provided treatment in cardiac arrest. Few drugs used in the treatment of cardiac arrest are supported by evidence. After starting CPR and attempting defibrillation, rescuers can establish intravenous access, considering drug administration, and then insert an advanced airway. As in the 2011 Guideline, the 2015 Guideline combines the treatment processes of cardiac arrest into a universal algorithm; this also corresponds to the “megacode concept” used in ALS education. In other words, because changes in ECG rhythms may occur during ALS provided for cardiac arrest, a combined algorithm, rather than separate algorithms for each ECG rhythm, can be more effectively used in clinical field. For instance, the scenario in which “VF occurs while treating asystole, and spontaneous circulation is recovered after defibrillation,” could occur in practice; in such cases, if VF is observed while treating asystole, the treatment direction should change to treat VF first. 44 The treatment of cardiac arrest starts with BLS. BLS includes the recognition of the patient, confirmation of cardiac arrest, call for help, and immediate beginning CPR. Regardless of the ECG rhythm, push hard and fast and release completely in chest compression. Moreover, to minimize the fatigue of the chest compressors, the CPR team leader should switch the roles with the compressor approximately every 2 minutes (or after 5 cycles of compressions and ventilations at a ratio of 30:2). Healthcare providers should interrupt chest compressions as infrequently as possible and try to limit interruptions to no longer than 10 seconds except for specific interventions such as use of a defibrillator or analyzing the ECG rhythms through monitors, confirmation of pulse for confirmation of spontaneous circulation (when perfusing rhythm appears on ECG), and insertion of an advanced airway. As ways to evaluate the effectiveness and quality of CPR, there are a number of methods and emerging technologies to monitor the patient during CPR and potentially help guide ALS interventions (e.g. monitoring of ETCO2 partial pressure, diastolic arterial pressure, and central venous oxygen saturation). When an advanced airway is not in placement, chest compression and rescue ventilation should to be conducted in a 30:2 ratio; when the advanced airway is secured, chest compression should be conducted at 100-120 times/minute while ventilation should be conducted once in 6 seconds (10 times/minute).21 Hyperventilation should be avoided. Manual defibrillators, rather than automated defibrillators, are used in ALS to confirm ECG rhythms and to defibrillate. Although administration of drugs before conducting advanced airway management is recommended, depending on the team members' skills as well as the ongoing experience in inserting the airway and verifying proper position with minimal interruption of chest compression, drug administration and advanced airway management can be conducted simultaneously. In patients with an initial shockable rhythm, administration of epinephrine (intravenous or intraosseous injection) immediately after the first shock is recommended. In cases of asystole or PEA (non-shockable rhythms), early administration of epinephrine can increase the ROSC, survival to hospital discharge, and neurologically intact survival.34-36 This section discusses in detail the general management of patients experiencing cardiac arrest and provides an overview of the ALS Cardiac Arrest Algorithm (Figure 3-1)(Table 3-1). 45 Figure 3-1. Adult advanced life support algorithm. ECG: electrocardiography, CPR: cardiopulmonary resuscitation, VF: ventricular fibrillation, VT: ventricular tachycardia, IV: intravenous, IO: intraosseous, ETCO2: end-tidal carbon dioxide Table 3-1. Reference table of the adult advanced life support algorithm. Core ALS concepts Details Assess ECG rhythm Rotate a compressor and analyze rhythm every 2 minutes Defibrillation Biphasic: - initial dose 120 to 200 J (manufacturer recommendation) - refractory VF/pulseless VT: escalating doses Monophasic: 360 J Chest compression Push hard (5cm) and fast (100-120/min) 46 Ensure high quality chest compressions Start compression within 5 sec after defibrillation Use waveform capnography (achieve ETCO2 > 10 mmHg after endotracheal intubation or 20 min of CPR) Advanced airway management and ventilation Keep bag-valve-mask ventilation until advanced airway in place Perform endotracheal intubation or use a supraglottic airway Give 1 breath every 6 sec (10 breaths/min) with continuous chest compressions Avoid hyperventilation Drug administration (IV/IO) All cardiac arrest Epinephrine: 1 mg every 3-5 minutes ( every two CPR cycle as equal to 4 minutes) Vasopressin: 40 IU (replace first or second dose of epinephrine) - Hospitals that already use vasopressin may continue to use - Bundled regimen of epinephrine, vasopressin and steroid may be considered in in-hospital cardiac arrest Refractory VF/pulseless VT Amiodarone: 300 mg bolus (first dose), 150 mg (second dose) Lidocaine (as an alternative if amiodarone is not available) : 1-1.5mg/kg (first dose), 0.5-0.75 mg/kg (second dose) Treat reversible causes Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypothermia Hypo/hyperkalemia, Tension pneumothorax, Toxins, Tamponadecardiac, Thrombosis-coronary or pulmonary Consider additional CPR modalities Ultrasound imaging Mechanical chest compressions Extracorporeal CPR ALS, advanced life support; ECG, electrocardiography; VT, ventricular tachycardia; VF, ventricular fibrillation; ETCO2, end-tidal carbon dioxide; IV, intravenous; IO, intraosseous; CPR, cardiopulmonary resuscitation, 1. Shockable rhythms (VF/pulseless VT) 47 Because VF and pulseless VT can be treated with defibrillation, they are referred to as shockable rhythms. The most important treatment for VF or pulseless VT is immediate bystander CPR and defibrillation as soon as possible. When VF is found on ECG monitor during CPR, providers should deliver one shock (biphasic defibrillator: 120-200J, monophasic defibrillator: 360J) and then resume CPR immediately for 2 minutes, beginning with chest compressions without pulse check or ECG rhythm confirmation. When the defibrillation energy dose recommended by the manufacturer is not known, defibrillation should be conducted at 200J when a biphasic defibrillator is used. During chest compression, an intravenous or intraosseous route for drug administration should be established. ECG rhythms should be checked after two minutes of CPR. If VF persists, the second and subsequent energy doses should be equivalent, and higher doses may be considered.37, 38 The entire process of manual defibrillation should be achievable in less than a 5-second interruption to chest compression.39, 40 During chest compression, epinephrine should be injected, and bolus IV fluids need to be pushed through the site of injection immediately. Meanwhile, another rescuer should perform advanced airway management. After two minutes of chest compressions, analyze the rhythm and deliver another shock immediately if indicated. Although 1 mg of epinephrine should be administered every 3 to 5 minutes in principle, it can be administered every two CPR cycles (4 minutes when rescuers take turns in conducting chest compression every two minutes).When VF/pulseless VT persists after 2 to 3 shocks, consider administering an antiarrhythmic such as amiodarone. 300 mg of amiodarone is recommended as the first dose; when VF/pulseless VT persists, additional 150 mg can be administered after 4 minutes from initial administration. If amiodarone is not available, lidocaine may be considered as an alternative. Although the previous 2011 Guidelines suggested consideration of magnesium administration for refractory VF, the new Guidelines do not recommend routine use of magnesium any more, as it does not result in any improvement in survival prognosis.41 If the ECG rhythms change to asystole or PEA while treating for VF/pulseless VT, the treatment should proceed according to the algorithm for non-shockable rhythms. 2. Non-shockable rhythms (PEA and asystole) 48 Asystole refers to ventricular asystole; PEA is a heterogeneous group of pulseless rhythms that includes pseudo-electromechanical dissociation (pseudo-EMD), idioventricular rhythms, ventricular escape rhythms, and bradyasystolic rhythms. As asystole and PEA do not require defibrillation during CPR, they are referred to as "non-shockable rhythms." PEA is often caused by reversible conditions and can be treated if those conditions are identified and corrected. Typical examples of such reversible causes are often referred to as the “5Hs and 5Ts”: hypovolemic shock, hypoxia, hyperkalemia or hypokalemia, hydrogen ions (metabolic acidosis), hypothermia (the 5Hs), thromboembolism of the pulmonary artery (pulmonary embolism), thrombosis of the coronary artery (myocardial infarction), tension pneumothorax, cardiac tamponade, and toxins (the 5Ts). Survival from cardiac arrest with asystole is poor. Of note, the hope for resuscitation is to identify and treat a reversible cause of non-shockable rhythms. If the ECG rhythm is non-shockable, chest compression should be immediately performed for 2 minutes. If the QRS complex can be confirmed in PEA, the pulse should be quickly checked. If there is no pulse, CPR should be conducted for 2 minutes while the route (intravenous or intraosseous) for drug administration is established. Epinephrine should be administered every 3 to 5 minutes or every two CPR cycles (4 minutes). After 2 minutes of chest compression, rhythms should be analyzed. If asystole or PEA persists, chest compression should be continued, and then advanced airway management should be conducted. Atropine is no longer used in treatment of asystole. 3. Immediate post-cardiac arrest treatment Post-cardiac arrest care is offered to patients whose spontaneous circulation has recovered as a result of ALS care. Integrated post-cardiac arrest treatment, which includes hemodynamic stabilization, adequate ventilation and controlling of blood oxygen saturation, TTM, and PCI for acute coronary syndrome, should be provided immediately after the recovery of spontaneous circulation. 4. In-hospital resuscitation 49 For all in-hospital cardiac arrests, cardiopulmonary arrest should be recognized immediately and CPR should be started immediately; if indicated, defibrillation is attempted as soon as possible and certainly within 3 minutes. The importance of “prevention and early detection of cardiac arrest,” which is the first link suggested in the 2015 CPR Guidelines, is emphasized not only in out-of-hospital cardiac arrest, but also in in-hospital cardiac arrest. The resuscitation team may take the form of a traditional CPR team, which is called only when cardiac arrest is detected. Alternatively, hospitals may have strategies to engage rapid response teams (RRTs) or medical emergency teams (METs) to recognize patients at risk of cardiac arrest before cardiac arrest occurs.16, 42, 43 Contrary to out-of-hospital cardiac arrest, vasopressin may provide some benefit when bundled with epinephrine and steroid in treating in-hospital cardiac arrests.30, 31 Monitoring during ALS Monitoring both provider performance and patient physiologic parameters during CPR is essential to optimizing CPR quality and feedback on the effectiveness of chest compression.44 ETCO2 partial pressure, coronary perfusion pressure, and central venous oxygen saturation can be used as physiological monitoring indices during ALS. It is recommended to use quantitative waveform capnography in intubated patients to monitor CPR quality, optimize chest compressions, detect ROSC during chest compression or when rhythm check reveals an organized rhythm, and confirmation of the location of endotracheal intubation.25, 26, 29 Although placement of invasive monitors during CPR is not generally warranted, physiologic parameters such as arterial pressures and central venous oxygen saturation, when available, may also be helpful in optimizing CPR and detecting ROSC. The main determinant of ETCO2 during CPR is perfusion to the lungs. Persistently low ETCO2 values < 10 mm Hg during CPR in intubated patients suggest that ROSC is unlikely. Monitoring the ETCO2 during ALS can help in maintaining high-quality chest compression and detecting compressor fatigue.45, 46 If the ETCO2 partial pressure is measured to be less than 10 mm Hg, the quality of ALS should be improved by increasing performance or changing a compressor. If ETCO2 abruptly increases to a normal value of 35 to 40 mm Hg, it is reasonable to consider this an indicator of ROSC. Continued insufficient ETCO2 (<10mmHg) after intubation 50 and 20 minutes after the initial resuscitation is associated with extremely poor chances for ROSC and survival outcomes.26, 27, 47 In non-intubated patients (those with bag-mask ventilation or supraglottic airway), ETCO2 may not consistently reflect the true value, making the measurement less reliable as a prognostic tool.1 However, the measurement of ETCO2 partial pressure should not be used as the single index to monitor the quality of ALS or to predict the recovery of spontaneous circulation. Medications for cardiac arrest High-quality CPR and rapid defibrillation are most important in cardiac arrest, and drug administration is considered next. After starting CPR and conducting defibrillation, intravenous or intraosseous access has been established for drug administration. The establishment of peripheral access is preferred because it does not require interruption of chest compression. In cases of shockable rhythms, defibrillation should be conducted first, and epinephrine administration follows afterward; in cases of non-shockable rhythms, drugs should be administered immediately and early once chest compression begins and once the intravenous route is achieved.36 1. Epinephrine Epinephrine is the universal vasopressor used in cardiac arrest treatment. Epinephrine stimulates adrenergic receptors, produces vasoconstriction, increases blood pressure and heart rate, and improves perfusion pressure to the brain and heart. Based on improvements in short-term prognosis resulting from epinephrine as compared to placebo, administration of standard dose of epinephrine to cardiac arrest patients is recommended. However, it is not recommended to add vasopressin to standard-dose epinephrine. High-dose epinephrine is not recommended for routine use in cardiac arrest.48 Standard-dose epinephrine (1 mg every 3 to 5 minutes) is recommended for patients experiencing cardiac arrest. The standard protocol used during CPR for adults is as follows: 1 mg of epinephrine is administered quickly in the form of a 1:1,000 ampule or 1:10,000 prefilled syringe formula every 3 to 5 minutes or every two cycles of chest compression rotation (4 minutes).49, 50 Either intravenous or intraosseous routes can be used. If IV/IO access is delayed or cannot be established, epinephrine may be given by the endotracheal route at a dose of 2 to 2.5 mg.51 51 The timing of epinephrine administration during CPR depends on the cardiac arrest rhythm. In cardiac arrest patients with a non-shockable rhythm, early administration of epinephrine is suggested.34 Optimal timing of epinephrine cannot be recommended because of insufficient evidence, particularly in relation to defibrillation in cardiac arrest due to a shockable rhythm. In such cases, early defibrillation, rather than the timing of epinephrine administration, should be considered first, and epinephrine is quickly administered after that.34, 36 2. Vasopressin Vasopressin is a non-adrenergic peripheral vasoconstrictor that increases arterial blood pressure. Vasopressin offers no advantage as a substitute for epinephrine in out-of-hospital cardiac arrest. The use of vasopressin in treatment of out-of-hospital cardiac arrest as an alternative to epinephrine is no longer recommended. However, those healthcare professionals working in systems that already use vasopressin may continue to do so because there is no evidence of harm from using vasopressin when compared to epinephrine.47 Considering that vasopressin is currently being used in cases of in-hospital cardiac arrest, the evidence to support changing the existing guideline is also lacking. The effect of vasopressin in cardiac arrest does not differ from that of epinephrine; therefore, 40 units of vasopressin can be administered once through an intravenous or intraosseous route to replace the first or second epinephrine administration.52 Moreover, the “vasopressor bundle” combination therapy, which combines steroids, epinephrine, and vasopressin, is being suggested as a treatment option for in-hospital cardiac arrest.30, 31 3. Antiarrhythmic drug Although the survival to hospital admission rate was reported to increase in a study that investigated the effectiveness of antiarrhythmic drugs in refractory VF/pulseless VT, no antiarrhythmic drug has yet been shown to increase long-term survival or neurologic outcome after cardiac arrest due to VF/pulseless VT.53 Amiodarone, however, has been shown to increase short-term survival to hospital admission when compared with placebo or lidocaine.54 Although the use of magnesium was recommended until the 2011 Guidelines when hypomagnesemia was suspected in patients with cardiac arrest, the new Guidelines do not recommend routine use of magnesium for adult VF/pulseless VT patients.41 1) Amiodarone 52 IV amiodarone affects sodium, potassium, and calcium channels as well as α- and β-adrenergic blocking actions. Amiodarone is used to treat refractory VF/pulseless VT that does not respond to defibrillation. The initial dose of 300 mg can be injected intravenously or intraosseously; if there is no response, a second dose of 150 mg amiodarone is administered after two cycles of chest compression rotation (after 4 minutes).55 2) Lidocaine The short- or long-term effects of lidocaine in refractory ventricular fibrillation/pulseless ventricular tachycardia that does not respond to defibrillation or repeats after defibrillation have been investigated in only a limited number of studies.56, 57 Lidocaine can be considered in cases where amiodarone is not available.54 The initial dose is 1 to 1.5 mg/kg IV/IO. Repeat if indicated at 0.5 to 0.75 mg/kg over 5- to 10-minute intervals to a maximum of 3 mg/kg. Additional considerations during ALS 1. Oxygen supply during CPR A study on out-of-hospital cardiac arrest analyzed outcome according the arterial oxygen partial pressure during CPR and reported that the survival-to-hospital admission rate increased in the group that received high concentration of oxygen.58 When supplementary oxygen is available, it may be reasonable to use the maximal feasible inspiratory concentration during CPR. After the recovery of spontaneous circulation, it is recommended to administer the maximum oxygen concentration that can maintain the arterial oxygen saturation above 94%. 2. Factors that predict the prognosis during CPR The ETCO2, which reflects the cardiac output induced by chest compression, is the only predicting factor currently being used during CPR. Survival prognosis was found to be poor in studies that investigated inhospital and out-of-hospital cardiac arrest when ETCO2 was maintained at less than 10 mm Hg in cardiac arrest patients with endotracheal intubation even 20 minutes after the start of CPR.26, 27 Hence, an ETCO2 less than 10 mm Hg immediately after intubation and 20 minutes after the initial resuscitation is associated with extremely 53 poor chances for ROSC and survival.47 The ETCO2 below 10 mm Hg that persists even after 20 minutes of appropriate ALS can be used as a criterion, in association with other various factors, to stop ALS. The ETCO2 should not be used alone as an indication to terminate resuscitation efforts. This index cannot be applied in patients that do not have endotracheal intubation. In cases of a simple non-waveform capnography used in prehospital care, the measurements can be used to confirm endotracheal intubation. However, these are not recommended for prognostication of survival or as evidence for stopping CPR. Multimodal approach to decision of terminating resuscitation may be required during CPR. 3. Application of ultrasonography during CPR The evidence supporting the effects of ultrasonography used during adult CPR is not sufficient. However, the use of ultrasonography may be considered to determine the reversible causes of cardiac arrest only in cases that ultrasonography would not interfere with CPR.59 Although no evidence supports that the use of echocardiography improves the prognosis of cardiac arrest patients, it can help in diagnosing the cause of treatable cardiac arrest, including cardiac tamponade, pulmonary thromboembolism, myocardial infarction, and aortic dissection. Moreover, it can also be used as an alternative of ETCO2 capnography to confirm the location of endotracheal intubation during CPR.60 4. The use of mechanical chest compression devices Automated mechanical chest compression devices use a piston that compresses the sternum, a band that tightens the thorax, or both to conduct CPR. Since the announcement of the 2005 Guidelines, important clinical studies that used mechanical chest compression devices were conducted. As the evidence supporting effectiveness of mechanical chest compression devices over manual CPR is insufficient yet, manual chest compression remains the standard care for cardiac arrest.5, 32, 33 However, mechanical chest compression devices can be used as reasonable alternatives in the following cases: when the conventional chest compression is not possible, when high-quality chest compression cannot be conducted due to the prolonged CPR, and when there is a lack of medical personnel required for CPR. In particular, in certain circumstances, such as inside a moving ambulance, inside angiography rooms, during prolonged CPR, and during ECPR, the use of mechanical chest compression devices can be considered as a reasonable alternative to high-quality chest 54 compression. 5. Extracorporeal CPR Extracorporeal CPR (ECPR) maintains artificial circulation using extracorporeal devices in patients with cardiac arrest who do not response to conventional CPR. It is known to exert positive influences on the survival and neurological prognosis of adult cardiac arrest patients; therefore, it can be used in selective circumstances.6, 7, 61 As cannula and devices should be inserted into large arteries and veins while conducting CPR, special equipment and trained members are required. ECPR is a complex intervention that requires a highly trained team, specialized equipment, and multidisciplinary support. Only for selected patients who have a cardiac arrest and for whom the suspected etiology of cardiac arrest is potentially reversible, ECPR may be considered as an alternative to conventional CPR.6, 7 55 References 1. Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult Advanced Cardiovascular Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergenc y Cardiovascular Care. Circulation 2015;132:S444-64. 2. Hanif MA, Kaji AH, Niemann JT. Advanced airway management does not improve outcome of out -of-hospital cardiac arrest. Acad Emerg Med 2010;17:926-31. 3. Hasegawa K, Hiraide A, Chang Y, Brown DF. Association of prehospital advanced airway manage ment with neurologic outcome and survival in patients with out-of-hospital cardiac arrest. JAMA 2013; 309:257-66. 4. McMullan J, Gerecht R, Bonomo J, et al. Airway management and out-of-hospital cardiac arrest ou tcome in the CARES registry. Resuscitation 2014;85:617-22. 5. 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Emergency coronary angiography in comatose c ardiac arrest patients: do real-life experiences support the guidelines? Eur Heart J Acute Cardiovasc C are 2012;1:291-301. 15. O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiolog y Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013;127:529- 55. 16. Maharaj R, Raffaele I, Wendon J. Rapid response systems: a systematic review and meta-analysis. Crit Care 2015;19:254. 17. Stiell IG, Brown SP, Nichol G, et al. What is the optimal chest compression depth during out-ofhospital cardiac arrest resuscitation of adult patients? Circulation 2014;130:1962-70. 18. Idris AH, Guffey D, Pepe PE, et al. Chest compression rates and survival following out-of-hospita l cardiac arrest. Crit Care Med 2015;43:840-8. 19. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilation-induced hypotension during car diopulmonary resuscitation. Circulation 2004;109:1960-5. 20. O'Neill JF, Deakin CD. Do we hyperventilate cardiac arrest patients? Resuscitation 2007;73:82-5. 21. Abella BS, Alvarado JP, Myklebust H, et al. Quality of cardiopulmonary resuscitation during in-h ospital cardiac arrest. JAMA 2005;293:305-10. 22. Cook TM, Kelly FE. Time to abandon the 'vintage' laryngeal mask airway and adopt second-gener ation supraglottic airway devices as first choice. Br J Anesth 2015;115:497-9. 23. Sunde GA, Brattebo G, Odegarden T, Kjernlie DF, Rodne E, Heltne JK. Laryngeal tube use in o ut-of-hospital cardiac arrest by paramedics in Norway. Scand J Trauma Resusc Emerg Med 2012;20:84. 57 24. Duckett J, Fell P, Han K, Kimber C, Taylor C. Introduction of the I-gel supraglottic airway devic e for prehospital airway management in a UK ambulance service. Emerg Med J 2014;31:505-7. 25. Pearce AK, Davis DP, Minokadeh A, Sell RE. Initial end-tidal carbon dioxide as a prognostic ind icator for inpatient PEA arrest. Resuscitation 2015;92:77-81. 26. Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide and outcome of out-of-hospital cardi ac arrest. N Engl J Med 1997;337:301-6. 27. Ahrens T, Schallom L, Bettorf K, et al. End-tidal carbon dioxide measurements as a prognostic in dicator of outcome in cardiac arrest. American journal of critical care : an official publication, Am J Crit Care 2001;10:391-8. 28. Silvestri S, Ralls GA, Krauss B, et al. The effectiveness of out-of-hospital use of continuous endtidal carbon dioxide monitoring on the rate of unrecognized misplaced intubation within a regional em ergency medical services system. Ann Emerg Med 2005;45:497-503. 29. Grmec S. Comparison of three different methods to confirm tracheal tube placement in emergency intubation. Intensive Care Med 2002;28:701-4. 30. Mentzelopoulos SD, Zakynthinos SG, Tzoufi M, et al. Vasopressin, epinephrine, and corticosteroid s for in-hospital cardiac arrest. Arch Intern Med 2009;169:15-24. 31. Mentzelopoulos SD, Malachias S, Chamos C, et al. Vasopressin, steroids, and epinephrine and neu rologically favorable survival after in-hospital cardiac arrest: a randomized clinical trial. JAMA 2013;3 10:270-9. 32. Rubertsson S, Lindgren E, Smekal D, et al. Mechanical chest compressions and simultaneous defi brillation vs conventional cardiopulmonary resuscitation in out-of-hospital cardiac arrest: the LINC rand omized trial. JAMA 2014;311:53-61. 33. Perkins GD, Lall R, Quinn T, et al. Mechanical versus manual chest compression for out-of-hospi tal cardiac arrest (PARAMEDIC): a pragmatic, cluster randomised controlled trial. Lancet 2015;385:947 -55. 34. Donnino MW, Salciccioli JD, Howell MD, et al. Time to administration of epinephrine and outco me after in-hospital cardiac arrest with non-shockable rhythms: retrospective analysis of large in-hospit al data registry. BMJ 2014;348:g3028. 58 35. Goto Y, Maeda T, Goto Y. Effects of prehospital epinephrine during out-of-hospital cardiac arrest with initial non-shockable rhythm: an observational cohort study. Crit Care 2013;17:R188. 36. Koscik C, Pinawin A, McGovern H, et al. Rapid epinephrine administration improves early outco mes in out-of-hospital cardiac arrest. Resuscitation 2013;84:915-20. 37. Stiell IG, Walker RG, Nesbitt LP, et al. BIPHASIC Trial: a randomized comparison of fixed low er versus escalating higher energy levels for defibrillation in out-of-hospital cardiac arrest. Circulation 2007;115:1511-7. 38. Koster RW, Walker RG, Chapman FW. Recurrent ventricular fibrillation during advanced life supp ort care of patients with prehospital cardiac arrest. Resuscitation 2008;78:252-7. 39. Cheskes S, Schmicker RH, Verbeek PR, et al. The impact of peri-shock pause on survival from o ut-of-hospital shockable cardiac arrest during the Resuscitation Outcomes Consortium PRIMED trial. R esuscitation 2014;85:336-42. 40. Sell RE, Sarno R, Lawrence B, et al. Minimizing pre- and post-defibrillation pauses increases the likelihood of return of spontaneous circulation (ROSC). Resuscitation 2010;81:822-5. 41. Thel MC, Armstrong AL, McNulty SE, Califf RM, O'Connor CM. Randomised trial of magnesiu m in in-hospital cardiac arrest. Duke Internal Medicine Housestaff. Lancet 1997;350:1272-6. 42. Shin TG, Jo IJ, Song HG, Sim MS, Song KJ. Improving survival rate of patients with in-hospital cardiac arrest: five years of experience in a single center in Korea. J Korean Med Sci 2012;27:146-5 2. 43. Kwak HJ, Yun I, Kim SH, et al. The extended rapid response system: 1-year experience in a uni versity hospital. J Korean Med Sci 2014;29:423-30. 44. Crowe C, Bobrow BJ, Vadeboncoeur TF, et al. Measuring and improving cardiopulmonary resuscit ation quality inside the emergency department. Resuscitation 2015;93:8-13. 45. Hamrick JL, Hamrick JT, Lee JK, Lee BH, Koehler RC, Shaffner DH. Efficacy of chest compres sions directed by end-tidal CO2 feedback in a pediatric resuscitation model of basic life support. J A m Heart Assoc 2014;3:e000450. 46. Genbrugge C, Meex I, Boer W, et al. Increase in cerebral oxygenation during advanced life suppo rt in out-of-hospital patients is associated with return of spontaneous circulation. Crit Care 2015;19:11 59 2. 47. Soar J, Callaway CW, Aibiki M, et al. Part 4: Advanced life support: 2015 International Consens us on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Rec ommendations. Resuscitation 2015;95:e71-120. 48. Callaham M, Madsen CD, Barton CW, Saunders CE, Pointer J. A randomized clinical trial of hig h-dose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest. JAM A 1992;268:2667-72. 49. Helm C, Gillett M. Adrenaline in cardiac arrest: Prefilled syringes are faster. Emerg Med Australa s 2015;27:312-6. 50. Moreira ME, Hernandez C, Stevens AD, et al. Color-Coded Prefilled Medication Syringes Decreas e Time to Delivery and Dosing Error in Simulated Emergency Department Pediatric Resuscitations. An n Emerg Med 2015;66:97-106 e3. 51. Neumar RW, Otto CW, Link MS, et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascul ar Care. Circulation 2010;122:S729-67. 52. Hess EP, Russell JK, Liu PY, White RD. A high peak current 150-J fixed-energy defibrillation pr otocol treats recurrent ventricular fibrillation (VF) as effectively as initial VF. Resuscitation 2008;79:28 -33. 53. Kudenchuk PJ, Cobb LA, Copass MK, et al. Amiodarone for resuscitation after out-of-hospital car diac arrest due to ventricular fibrillation. N Engl J Med 1999;341:871-8. 54. Dorian P, Cass D, Schwartz B, Cooper R, Gelaznikas R, Barr A. Amiodarone as compared with l idocaine for shock-resistant ventricular fibrillation. N Engl J Med 2002;346:884-90. 55. Soar J, Nolan JP, Bottiger BW, et al. European Resuscitation Council Guidelines for Resuscitation 2015: Section 3. Adult advanced life support. Resuscitation 2015;95:100-47. 56. Herlitz J, Ekstrom L, Wennerblom B, et al. Lidocaine in out-of-hospital ventricular fibrillation. Do es it improve survival? Resuscitation 1997;33:199-205. 57. Harrison EE. Lidocaine in prehospital countershock refractory ventricular fibrillation. Ann Emerg Med 1981;10:420-3. 60 58. Spindelboeck W, Schindler O, Moser A, et al. Increasing arterial oxygen partial pressure during c ardiopulmonary resuscitation is associated with improved rates of hospital admission. Resuscitation 201 3;84:770-5. 59. Breitkreutz R, Price S, Steiger HV, et al. Focused echocardiographic evaluation in life support and peri-resuscitation of emergency patients: a prospective trial. Resuscitation 2010;81:1527-33. 60. Chou HC, Chong KM, Sim SS, et al. Real-time tracheal ultrasonography for confirmation of endo tracheal tube placement during cardiopulmonary resuscitation. Resuscitation 2013;84:1708-12. 61. Maekawa K, Tanno K, Hase M, Mori K, Asai Y. Extracorporeal cardiopulmonary resuscitation for patients with out-of-hospital cardiac arrest of cardiac origin: a propensity-matched study and predictor analysis. Crit Care Med 2013;41:1186-96. 61 Part 4. Post-Cardiac Arrest Care High quality integrated post-cardiac arrest care can significantly influence the outcome of patients with cardiac arrest, especially neurological recovery, and numerous studies have been conducted on this topic. In the 2015 Korean cardiopulmonary resuscitation (CPR) guidelines, post-cardiac arrest care was emphasized with effective advanced life support as one of the essential chains for survival. Based on an in-depth scientific evidence review using a standardized methodological approach proposed by the GRADE working group, the guidelines either partially updated the recommendations or added new recommendations for each specific topic. Post-cardiac arrest care strategies (Figure 4-1, Table 4-1) 62 Figure 4-1. Post-cardiac arrest care algorithm ECG, electrocardiography; SBP, systolic blood pressure; MAP, mean arterial pressure; PCI, percutaneous coronary intervention; ACS, acute coronary syndrome Table 4-1. ABCs in adult immediate post-cardiac arrest care Strategy Doses/Details 63 Airway Consider tracheal intubation and waveform capnography Breathing - Oxygenation Avoid hypoxemia Goal: Titrate FiO2 to achieve SpO2 94–98% Breathing - Ventilation Avoid excessive ventilation Goal: Titrate to target PaCO2 35–45 mm Hg or PETCO2 30–40 mm Hg Circulation - Hemodynamics Avoiding and immediately correcting hypotension (systolic blood pressure < 90 mm Hg; mean arterial pressure < 65 mm Hg) Goal: Systolic blood pressure ≥ 100 mm Hg Circulation - Vasoactive drugs Norepinephrine: 0.1–0.5 mcg/kg/min Dopamine: 5–10 mcg/kg/min Epinephrine: 0.1–0.5 mcg/kg/min Correct the reversible causes Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypokalemia/hyperkalemia, Hypothermia, Tension pneumothorax, cardiac Tamponade, Toxins, pulmonary Thrombosis, coronary Thrombosis 64 1. Airway and breathing When a patient is unconscious after the return of spontaneous circulation (ROSC), the airway should b e secured by tracheal intubation, and this should be confirmed by measuring the end-tidal carbon dioxi de (ETCO2) and oxygen saturation (SpO2) levels using waveform capnography and pulse oximetry; addi tionally, mechanical ventilation should be performed while continuously monitoring the ETCO2 and SpO 2. To avoid hypoxia, it is reasonable to use the highest available oxygen concentration until appropriate monitoring is available to evaluate the arterial oxygen tension (PaCO2) or arterial oxygen saturation (S aO2) levels. When resources are available to titrate the fraction of inspired oxygen (FiO2) and monitor the saturation, it is reasonable to decrease the FiO2, provided that the SaO2 level can be maintained at the target range. A study based on a registry reported that hyperoxia within 24 hours after ROSC was associated wit h a poor outcome compared to hypoxemia or normoxemia within 24 hours.1 In another study, hyperoxi a was shown to have a dose-dependent relationship with poor outcomes, rather than with a certain thre shold level.2 In addition, hyperoxia was associated with poor prognosis in a study of patients with card iac arrest who had received mild therapeutic hypothermia.3 In contrast, a study of approximately 12,000 patients with cardiac arrest reported that there was no association between hyperoxia and mortality aft er the inspired oxygen level and disease severity were adjusted.4 A meta-analysis of 14 observational st udies showed significant heterogeneity across studies.5 Therefore, it is suggested to maintain the SaO2 a t a level of 94~98% to avoid hypoxemia and the potential risk of hyperoxia. Hypocapnia causes cerebral vasoconstriction, and it reduces cerebral blood flow.6 Observational studie s using a registry of patients with cardiac arrest have reported an association between hypocapnia and poor neurologic outcome.7,8 Two observational studies reported that mild hypercapnia was associated wit h more favorable neurologic outcomes in patients with cardiac arrest in intensive care units.7,9 However, several other studies did not show a consistent association between hypercapnia and outcome.7-10 There fore, it is suggested to maintain the CO2 level within a normal physiological range (PaCO2 35~45 mm Hg or ETCO2 30–40 mmHg). 2. Circulation 65 1) Hemodynamic stabilization Post-cardiac arrest patients are often hemodynamically unstable due to the underlying etiology of arrest, myocardial dysfunction, and systemic ischemia/reperfusion response.11 Therefore, immediately after ROSC, an arterial catheter should be promptly inserted, and the arterial blood pressure should be monitored continuously. If an arterial catheter cannot be inserted, the blood pressure should be frequently measured noninvasively until the patient becomes hemodynamically stable. Dobutamine can be helpful for post-cardiac arrest myocardial dysfunction.12 In addition, vasodilation occurs due to the systemic ischemia/reperfusion response; thus, dopamine or norepinephrine may be needed, and intravenous fluids can be an effective treatment depending on the situation.11 If hemodynamic instability persists even with the infusion of intravenous fluids or vasoactive drugs, a mechanical circulatory assistance device should be considered.13 Although there are observational studies of patients with cardiac arrest that have investigated the relationship between blood pressure and outcome, a controlled study has not been conducted on a target goal of blood pressure. An observational study examined whether treatment with a specific hemodynamic goal (e.g., a mean arterial pressure [MAP] >65 mmHg) would improve neurologic and functional outcome compared to treatment without a specific hemodynamic goal. The study reported that the mortality rate was higher and the functional recovery was lower in the patient group whose systolic blood pressure (SBP) was <90 mmHg after CPR compared to other patient groups whose SBP was ≥90 mmHg.14 Two retrospective studies reported that the survival rate decreased in patients who maintained an SBP <90 mmHg and <100 mmHg.15,16 As several beforeand- after studies have implemented a bundle of care, which included a blood pressure goal, the effect of blood pressure cannot be evaluated alone. Moreover, different studies have shown different results regarding a specific level of blood pressure, and the level of evidence from existing studies is insufficient to determine a target blood pressure goal. Seven studies have investigated the effect of a bundle of care on neurologic outcome, and they reported different results. Some studies have found no association between a specific target blood pressure and neurologic outcome. In one of the studies, a MAP >80 mmHg was a goal, and in another study, an intervention was performed when a goal of MAP was below 75 mmHg, and both of which reported that using a bundle of care, including a hemodynamic goal, was not associated with the neurologic outcome.17,18 In contrast, other 66 studies have found that a bundle of care that included a blood pressure goal improved the neurologic outcome. Two prospective observational studies have reported that maintaining a MAP >65 mmHg improved the neurologic outcome, and an additional study demonstrated that the neurologic outcome was better in the patient group who maintained a MAP >100 mmHg at 2 hours after ROSC, suggesting an association between MAP and the neurological outcome.19-21 Yet, another study reported that in patients with a good neurologic outcome, maintaining the time-weighted MAP over 70 mmHg was associated with the neurologic outcome.22 Two beforeand- after observational studies have investigated the effect of using a bundle of care on the survival rate. Both of these studies used a bundle with a MAP >80 mmHg and >65 mmHg as a goal, but there was no significant difference in the survival rate.17,20 Thus, the evidence is insufficient to determine a specific hemodynamic goal for post-cardiac arrest care. It is suggested that hypotension (SBP <90 mmHg or MAP <65 mmHg) should be immediately corrected, and a hemodynamic goal should be determined for individual patients, while maintaining an SBP >100 mmHg. 2) Evaluation and treatment of reversible causes After ROSC and during CPR, the resuscitation team should make efforts to evaluate the reversible caus es of cardiac arrest (i.e., the five H’s and five T’s: hypovolemia, hypoxia, hydrogen ions [acidosis], hy per/hypokalemia, hypothermia, thromboembolism, thrombosis, tension pneumothorax, cardiac tamponade, and tablets) and then treat the patient. (1) Intervention of acute coronary syndromes Acute coronary syndromes are a common cause of adult out-of-hospital cardiac arrest (OHCA) with no obvious extracardiac cause of arrest.23,24 Thus, a 12-lead ECG and a cardiac marker test should be obtained as soon as possible after ROSC to confirm the presence or absence of acute coronary syndromes.25,26 Coronary angiography should be performed emergently for patients with OHCA with suspected cardiac etiology and ST elevation on ECG, regardless of whether the patient is conscious.27-29 If acute coronary syndromes are highly suspected in patients with OHCA with suspected cardiac etiology but their ECG does not show ST elevation after ROSC, early coronary angiography should be considered, regardless of the consciousness status.30,31 67 (2) Treatment of pulmonary embolism When cardiac arrest due to pulmonary embolism is strongly suspected, chest computed tomography (C T) should be performed, if possible. If cardiac arrest due to pulmonary embolism is confirmed, thromb olytics can be administered, or surgical or percutaneous embolectomy can be performed.32-34 Treatments for optimizing neurological recovery 1. Temperature control 1) Prevention and treatment of hyperpyrexia Observational studies have reported an association between poor outcome and fever after ROSC in pati ents without targeted temperature management (TTM).35,36 Hyperpyrexia occurs in many patients after T TM. However, the optimal approach to subsequent TTM remains unknown. Several studies have reporte d conflicting conclusions regarding the association with outcome.36-38 Although the effect of hyperpyrexi a on the outcome of post-cardiac arrest patients is not proven, a poor outcome was associated with hy perpyrexia in comatose patients in whom cerebral damage was due to other causes such as cerebral he morrhage or infarct, and it is relatively easy to treat or prevent hyperthermia.39,40 Therefore, it is sugge sted to continuously prevent or treat fever in adult comatose patients after ROSC from cardiac arrest, r egardless of whether the patient received TTM. 2) Targeted temperature management (1) Indications and target temperature One randomized controlled trial (RCT) and a pseudo-randomized trial demonstrated that TTM of 32~34°C improved the neurological outcome at hospital discharge and at 6 months in adult patients with OHCA with a shockable cardiac rhythm.41,42 Therefore, OHCA with a shockable rhythm is a main indication for TTM. Regarding patients with OHCA with a non-shockable rhythm, no RCT was available. In a cohort study with a 68 very low level of evidence, there was an association between mild induced hypothermia and 6-month survival in patients with OHCA with a non-shockable rhythm. However, a meta-analysis of two other cohort studies did not determine an association between mild induced hypothermia (32~34°C) and an improvement in neurological results.43-46 For patients with in-hospital cardiac arrest, no RCT has been published. A retrospective cohort study of 1,836 patients found no association between mild induced hypothermia and survival or a functionally favorable status at hospital discharge.47 However, in this study, the implementation rate of TTM was very low, and the overall outcome of patients treated without TTM was poor; therefore, the aggressive implementation of TTM became necessary. Additionally, ultra-mild hypothermia (36°C) has been suggested as another target temperature since a large, well-conducted RCT compared the target temperature levels of 33°C and 36°C, as it found that the neurological outcome and survival at 6 months after ROSC were not improved when the temperature was controlled at 36°C versus 33°C.48 Based on the scientific evidence, regardless of the initial rhythm for TTM, it is recommended to select and maintain a constant temperature between 32°C and 36°C in adult patients with cardiac arrest who do not show a meaningful response to verbal commands after ROSC. When making this recommendation, the writing group considered the characteristics of the cardiac arrest population in Korea and that pulseless electrical activity or asystole (i.e., a non-shockable cardiac rhythm) is relatively more frequently observed as the initial arrest rhythm. However, it is unknown whether TTM with mild induced hypothermia (32~34°C) or ultra-mild hypothermia (36°C) is helpful to specific subgroups with cardiac arrest, thus additional studies are needed to shed light on this issue. (2) Initiation and duration of TTM Neuronal injury following transient global brain ischemia/reperfusion progresses for several days in a complex biochemical cascade. Mild induced hypothermia influences various stages during the process.49,50 In particular, oxidative stress, increased excitatory amino acids, and energy depletion occur immediately after ROSC and during cardiac arrest. Theoretically, it would be helpful if mild hypothermia is induced in patients with cardiac arrest as quickly as possible.51,52 For this reason, several studies have compared the prehospital induction of hypothermia and hospital induction of hypothermia. In all seven RCTs with a medium level of evidence, there was no significant difference between the groups in terms of a poor neurologic outcome or mortality.53-59 A 69 meta-analysis of seven studies also did not show differences in the mortality rate or poor neurologic outcome between the groups at hospital discharge.46 Accordingly, based on current scientific evidence, it cannot be concluded that the prehospital induction of TTM is better than induction at the hospital; hence, more conclusive follow-up studies are needed. A high quality interventional study is not yet available with which to determine an optimal duration of TTM after cardiac arrest. Therefore, based on the duration used in two of the largest aforementioned RCTs, it is reasonable to maintain TTM for at least 24 hours after achieving the target temperature.41,48 (3) Methods of inducing and/or maintaining TTM Diverse cooling methods are used to induce and maintain a target temperature, but there is no one best method. External surface cooling methods used widely in the past (e.g., a cooling blanket, ice packs, and a wet towel) are easy and convenient to use. However, they take longer to lower the patient’s core temperature, and they are difficult to maintain at a constant level, which adds to the medical staff’s high workload. Recently, body temperature control has become easier, as cooling equipment that use endovascular catheters and external cooling equipment that regulates temperature with an auto-feedback system have become available, but they are expensive. Hence, medical staff that plan to perform TTM should consider a variety of factors (e.g., the place to initiate the treatment, staff’s ability and experience, speed in induction, stability during maintenance and rewarming, mobility of the equipment, adverse events associated with specific equipment or techniques, convenience of using the equipment, cost, etc.), and the most optimal cooling technique should be chosen for individual patients.60 Cold crystalloid intravenous fluid infusion is relatively easy to induce hypothermia, and it has been widely used in prehospital settings or during resuscitation for convenience. However, according to a meta-analysis of four RCTs, when TTM was initiated in the prehospital setting using cold crystalloid intravenous fluid infusion, the risk for re-arrest increased.46 In addition, pulmonary edema was increased according to one large-scale RCT.58 Therefore, it is not recommended to perform routine prehospital cooling of a patient after ROSC with the rapid infusion of cold intravenous fluid. When TTM is performed, the patient’s core temperature should be continuously monitored in the esophagus, bladder, or pulmonary artery. The pulmonary artery is the most accurate, but it has a limitation because it 70 requires an invasive procedure. The axillary temperature or oral temperature is not appropriate for measuring changes in the core temperature, and tympanic temperature sensors are difficult to use for a long time and they are often inaccurate. The rectal temperature is commonly used, but there can be temperature gaps when hypothermia is induced rapidly; thus, careful monitoring is needed.61 Moreover, there is not enough evidence for an optimal speed of rewarming. Accordingly, it is sugge sted to rewarm at a speed of 0.25~0.5°C per hour, which has been used often in previous studies41,42,48, and maintain normothermia (36.5~37.5°C) up to 72 hours after ROSC in comatose patients even after normothermia is achieved. 2. Glucose control Hyperglycemia is associated with mortality and a poor neurologic outcome in patients who have been r esuscitated from cardiac arrest, and it should be appropriately controlled. There is little evidence about a target blood glucose level to improve the outcome of patients with cardiac arrest. An RCT found no difference in the 30-day mortality rate between the groups with a target blood glucose level of 72~10 8 mg/dL and 108~144 mg/dL.62 In a before-and-after study that used a bundle of care with a target bl ood glucose level of 90~144 mg/dL, the neurological outcome improved after implementing the bundle, but the effect could not be attributed only to the controlled blood glucose level.75 Applying the findin gs of these studies to cardiac arrest patients may not be appropriate, because they examined the effect of controlling blood glucose level in critically ill patients.64,65 Although is still controversy on how to c ontrol the blood glucose level in critically ill patients, the strict control of blood glucose was associate d with an increased occurrence of hypoglycemia.62 Therefore, the target range of 144~180 mmHg is su ggested to prevent hypoglycemia, although evidence so far is insufficient. Hyperglycemia >180 mmHg should be treated with an insulin infusion per the hospital’s protocol, and care should be taken to prev ent hypoglycemia (<80 mg/dL). If hypoglycemia occurs, it should be immediately corrected by administ ering a glucose solution. The blood glucose level, especially, fluctuates during the induction or rewarmi ng period; therefore, it is desirable to frequently test the patient’s blood glucose level. 3. Control of seizures 71 No study has directly compared patients treated for seizure with those not treated for seizure. Furthermore, there is no evidence thus far that a specific anticonvulsant or combination therapy with anticonvulsant drugs is helpful in comatose patients after cardiac arrest. Therefore, if seizure occurs or is suspected, an electroencephalogram (EEG) needs to be performed immediately to determine the presence of epileptiform activity. Non-convulsive seizures can occur while TTM is performed with a neuromuscular blocking drug; thus, if possible, an EEG should be continuously monitored, and the arterial blood gas level or change in vital signs (e.g., unexplained tachycardia) should be carefully observed.66 To control seizures, any commonly used anticonvulsant needs to be promptly injected. In a case of generalized seizure, benzodiazepine, phenytoin, sodium valproate, propofol, levetiracetam, phenobarbital, and similar drugs can be used alone or in combination with each other. In cases of myoclonus, clonazepam, sodium valproate, levetiracetam, propofol, etc. can be used alone or in combination with each other.67 Post-anoxic myoclonic status epilepticus may not respond well to anticonvulsants.68,69 Available evidence does not support the prophylactic administration of anticonvulsants. Therefore, the routine use of prophylactic anticonvulsants in post-cardiac arrest patients is not recommended. 4. Sedation In most post-cardiac arrest patients, mechanical ventilation should be maintained during post-cardiac arrest care, and sedatives or analgesics may have to be intermittently or continuously administered. If a patient is sedated while TTM is performed, the time required to reach to the target temperature can be reduced because shivering is prevented or reduced. Using a sedation protocol can be helpful in these cases. Sedation after ROSC is a commonly used treatment method, but the level of evidence is not sufficient to make a recommendation about the duration to administer a sedative or neuromuscular blocker in post-cardiac arrest patients. A meta-analysis of 44 studies reported on sedative drugs that were used while TTM was performed among 68 intensive care units in various countries found that a large variety of drugs were being used.70 From the analysis, it is impossible to know which drugs may be associated with outcome, but mainly the combination therapy of an opioid and sedative was used. It is recommended to maintain a sedative over a short duration of action as much as possible, but no study has analyzed the effect of using sedatives in patients after cardiac arrest or has suggested treatment strategies. One study has suggested that the continuous administration 72 of neuromuscular blockers may be associated with a low mortality rate.71 However, neuromuscular blockers interfere with clinical examinations, and they obscure the occurrence of seizure. Therefore, if a neuromuscular blocker is continuously administered, the EEG should be continuously monitored. Evaluation of neurological prognostication In the 2015 guidelines, studies of patients who had and had not received TTM were evaluated. These studies evaluated the diagnostic accuracy of clinical examination, electrophysiological studies, biomarkers, and imaging tests for predicting poor neurological outcome, and they recommended diagnostic tests with a false positive rate (FPR) close to 0% and a narrow 95% confidence interval (CI, 0~10%) as predictors. It is recommended to predict the neurologic outcome at least 72 hours after ROSC, particularly because in most cases, a sedative and a neuromuscular blocker are administered to comatose patients after cardiac arrest while TTM is performed. An additional recommendation is to use a multimodal approach rather than relying on a single test or finding. 1. Clinical examination For a clinical examination to predict a poor neurologic outcome within 72 hours after ROSC in comatose patients after cardiac arrest, the bilateral absence of pupillary light reflex, or the combination of the absence of pupillary light reflex and absence of corneal reflex is required in both patients with TTM (FPR 0 [0~3%]) and without TTM (FPR 0 [0~8%]).72-80 The lack of motor movement (M1) or extensor posturing (M2) to pain has a high FPR level (27% [12~48%]) for predicting a poor neurologic outcome in comatose patients who did not receive TTM after cardiac arrest, and a similar finding was observed in patients who received TTM.72,74-77,78-83 Therefore, it is suggested to not use motor movement to pain alone to predict poor neurologic outcomes. Although they have a high sensitivity level (74% [68~79%]), they can be used to confirm a patient’s poor neurologic outcome or predict a poor neurologic outcome in combination with other predictors. Myoclonus in comatose patients within 72 hours after cardiac arrest is associated with a high FPR (10–15%) 73 for predicting poor neurologic outcomes; thus, it is suggested to not use it alone. In contrast, status myoclonus, which occurs within 72 hours after cardiac arrest, predicts poor neurologic outcome with a high accuracy in cases with TTM (FPR 0% [0~4%]) and without TTM (FPR 0% [0~5%]).66,72,73,84-86 Therefore, it is useful when used in combination with other predictors. If there is residual sedation and paralysis still remains, the clinical examination can be delayed to minimize the possibility of false positives. Seventy-two hours after ROSC is suggested as the earliest time to predict a poor neurologic outcome. 2. Electrophysiological studies To predict poor neurologic outcome in comatose patients after cardiac arrest, regardless of using TTM, the use of the bilateral absence of N20 waveform recorded from somatosensory evoked potentials (SSEPs) (FPR 1% [0~3%]) is recommended 24~72 hours after cardiac arrest or after rewarming.73-76,81-83,87-91 An SSEP recording requires appropriate skills and experience, and efforts should be considered to avoid muscle artifacts or electrical interference from the environment of the emergency room or intensive care unit. A lack of EEG background reactivity can accurately predict poor neurologic outcome in comatose patients after cardiac arrest during TTM (FPR 2% [1~7%]) and within 72 hours after ROSC (FPR 0% [0–3%]).81,83,92,93 However, using the pattern of background reactivity on EEG has limitations, because they are operator dependent, unquantifiable, and lack standardization. Status epilepticus (i.e., a persistent seizure over 72 hours) is commonly associated with a poor neurologic outcome (FPR 0~6%), if it occurs during hypothermia or rewarming in patients who received TTM.66,94 EEG burst-suppression can show a recovery of consciousness, if it occurs for 24~48 hours after ROSC in patients who did not receive TTM, or during hypothermia in patients who received TTM.83,95, but persistent burst-suppression that occurs 72 hours after ROSC is always associated with a poor neurologic outcome.73,96 Therefore, it is suggested to use EEG predictors (e.g., the lack of EEG response to external stimulation, EEG burst-suppression after rewarming, and status epilepticus) after 72 hours after ROSC in combination with other predictors to predict a poor neurologic outcome in comatose patients after cardiac arrest, regardless of using TTM. To predict poor neurologic outcomes of patients who received TTM, burst-suppression observed in the continuous amplitude-integrated EEG recordings, status epilepticus, and lack of normal trace over 36 hours can 74 be used in combination with other predictors.97 3. Biomarkers A high level or increasing levels of neuron-specific enolase (NSE) measured at 48~72 hours after ROSC can be used in combination with other predictors to predict poor neurologic outcomes of comatose patients who received TTM after cardiac arrest.98-100 A careful approach is necessary when testing NSE to avoid a false positive result that can occur due to hemolysis, and it is recommended to sample various points in time as much as possible. Since different studies have reported different NSE thresholds to predict a poor neurologic outcome with 0% FPR, it is recommended to not use the serum levels of NSE and S100B alone. 4. Imaging tests Global cerebral edema and the marked reduction of the gray matter/white matter ratio (GWR) on CT obtained within 2 hours after ROSC can predict poor neurologic outcomes with 0% FPR in comatose patients who received TTM after cardiac arrest. However, different studies have reported different GWR thresholds with 0% FPR, depending on the measurement technique and the studied brain area.78,100,101 An extensive restriction of diffusion detected on brain magnetic resonance imaging (MRI) obtained 2~6 days after ROSC and quantitatively measured with an apparent diffusion coefficient (ADC) can predict poor neurologic outcomes with 0% FPR in comatose patients who received TTM after cardiac arrest.102,103 However, the ADC threshold value with 0% FPR is different among studies, depending on the studied brain area and the measurement technique. Therefore, it is recommended to use the marked reduction of the GWR on CT obtained within 2 hours after ROSC or the extensive restriction of diffusion on MRI obtained 2~6 days after ROSC in combination with other predictors to predict poor neurologic outcomes of comatose patients who received TTM after cardiac arrest. 5. Neurological prognostication algorithm (Figure 4-2) 75 Figure 4-2. Neurological prognostication algorithm N/Ex, neurological examination; CT, computed tomography; NSE, neuron specific enolase; SSEP, somatosensory evoked potential; DW-MRI, diffusion-weighted magnetic resonance imaging; EEG, electroencephalography; ROSC, return of spontaneous circulation; GWR, gray matter/white matter ratio In most post-cardiac arrest comatose patients, cerebral function recovery occurs within 72 hours after ROSC.86,104 However, there is a possibility of decreased accuracy of clinical examination due to the influence of sedatives and neuromuscular blockers administered during the application of TTM. First, it is important to exclude confounders (e.g., residual sedation and paralysis) that can impact clinical examination after 72 hours after ROSC and the completion of TTM. Second, 72 hours after ROSC, use the flowchart to differentiate comatose patients who show the absence of motor movement or extensor posturing to 76 pain. Third, confirm the bilateral absence of pupillary light reflex and bilateral absence of N20 waveform in SSEPs, which have a low FPR and high accuracy. If all three aforementioned conditions are met, a poor neurological outcome can be predicted with accuracy (FPR <5%, narrow 95% CI). Otherwise, observe patients for at least 24 hours and assess the following predictors of poor outcome. 1) A marked reduction of the GWR on brain CT obtained within 2 hours after ROSC; 2) the lack of normal trace in the amplitude-integrated EEG recording observed for >36 hours; 3) status myoclonus occurring within 72 hours after ROSC, 4) a high serum level of NSE measured 48~72 hours after the ROSC; 5) unreactive burstsuppression or status epilepticus on EEG 72 hours after ROSC; and 6) extensive restriction of diffusion on MRI obtained 2~6 days after ROSC. A poor neurologic outcome can be predicted if two of six factors are observed. Otherwise, the outcome can be determined based on various findings in combination or after additional observation. 77 References 1. Kilgannon JH, Jones AE, Shapiro NI, et al. Association between arterial hyperoxia following resuscitation from cardiac arrest and in-hospital mortality. JAMA 2010;303:2165-71. 2. Kilgannon JH, Jones AE, Parrillo JE, et al. Relationship between supranormal oxygen tension and outcome after resuscitation from cardiac arrest. Circulation 2011;123:2717-22. 3. Janz DR, Hollenbeck RD, Pollock JS, McPherson JA, Rice TW. Hyperoxia is associated with increased mortality in patients treated with mild therapeutic hypothermia after sudden cardiac arrest. Crit Care Med 2012;40:3135-9. 4. Bellomo R, Bailey M, Eastwood GM, et al. Arterial hyperoxia and in-hospital mortality after resuscitation from cardiac arrest. Crit Care 2011;15:R90. 5. Wang CH, Chang WT, Huang CH, et al. 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Pediatric Basic Life Support Pediatric basic life support (PBLS) is a major component of the emergency medical response to the pediatric victims with cardiac arrest, which should be adequately implemented for a series of survival processes. The pediatric chain of survival comprises five components, including prevention and early recognition of cardiac arrest, early access (activation of emergency medical system [EMS]), early high-quality cardiopulmonary resuscitation (CPR), early defibrillation, and effective advanced life support and post-cardiac arrest care (Figure 5-1). The first four processes of the survival chain correspond to PBLS. Similar to adults, in children, prompt and effective CPR is essential for the successful recovery of spontaneous circulation and good neurological outcomes. In children, the survival rate varies depending on the cause of the cardiac arrest. For a cardiac arrest due to an asphyxial arrest, the rate of neurologically normal survival is 70%, while the survival rate is 20-30% in the case of a cardiac arrest from ventricular fibrillation (VF).1 Neonate is defined as being hospital after birth. An infant is defined as being less than 1 year of age after neonatal period. PBLS guideline applies to children under 8 years of age except neonate for both of the lay rescuer and the health care provider. As cardiac arrest from asphyxial arrest is a lot more common in children compared to those due to VF, ventilation is extremely important in pediatric CPR. Figure 5-1. Pediatric chain of survival. The pediatric chain of survival comprises five components, including prevention and early recognition of cardiac arrest, early access (activation of emergency medical system), early high-quality cardiopulmonary resuscitation, early defibrillation, and effective advanced life support and postcardiac arrest care 87 Pediatric basic life support for lay rescuers The algorithm for CPR in infants and pediatric patients experiencing cardiac arrest is the same as that used in adults, signifying unification in the education and training as well as continuation of the existing the 2011 Korean CPR guidelines, according to which chest compressions are carried out followed by rescue breathing2-4. A flow diagram of PBLS for lay rescuers is shown in Figure 5-2. 88 Figure 5-2. Algorithm of pediatric basic life support for lay rescuers. AED, automated external defibrillator; CPR, cardiopulmonary resuscitation; ALS, advanced life support. 1. Safety of the rescuer and the patient When conducting CPR, the safety of the rescuer and patient must be confirmed at the current location. CPR may carry the risk of transmission of infectious diseases, but the actual risk to the rescuer is extremely low. 2. Determination of the unresponsiveness If an unresponsive patient is gasping or not breathing at all, the lay rescuer should understand that the patient is undergoing a cardiac arrest and requires CPR. The rescuer should lightly tap the patient and shout out “are you okay?” or call out the name of the patient if known. Then, the rescuer should promptly check whether the child has injuries or requires medical treatments. 3. Activation of the EMS If the patient shows no response to stimulation and if the rescuer is the only person present, the rescuer should shout for help. If someone else arrives for help, the rescuer should request him or her to make a call to 119 as well as find an automated external defibrillator (AED). If there is no one else nearby, the rescuer should make a rescue request to 119 promptly. If the rescuer has a personal cellular phone, the rescuer should promptly call 119 at the site itself, without leaving the child. The rescuer should let the 119 dispatcher know about the status of the unresponsive patient, request for an AED, and perform the next resuscitation steps by following instructions given by the dispatcher. If the patient shows no response to stimulation and if there are two or more witnesses, the first rescuer should start CPR immediately and the other should call an EMS and request for an AED. Most cases of cardiac arrests in children are due to asphyxial arrest rather than VF. Therefore, if there is only one rescuer without a cellular phone, the rescuer should perform CPR for the first 2 minutes then call an EMS 89 and bring a nearby AED. The rescuer should return to the patient as soon as possible and use the AED. If no AED can be found, the rescuer should resume CPR starting with chest compression. 4. Checking patient breathing If a patient is confirmed to be breathing regularly, the child is not in need of CPR. In such cases, after confirming that there is no evidence of physical injuries, the rescuer should turn the child onto one side and into the recovery position to keep their airway open and reduce the risk of aspiration. The breathing status of the patient should be checked continuously until the arrival of the EMS. If the child tries to change his or her position into a more relaxed position, the child should be allowed to do so. If a patient is not responding to stimulation and not is breathing or only gasping (cardiac arrest breathing), CPR should be started. In some cases, patients who are in need of CPR and gasping can be mistaken as having normal breathing. Patients who are gasping should be regarded as not breathing, for which CPR should be started. 5. Chest compression In CPR, adequate chest compression maintains blood flow to vital organs and increases the possibility of recovery of spontaneous circulation. If a child is neither responding to stimulation nor breathing, the rescuer should immediately perform chest compression 30 times. Chest compression should be performed at a speed of 100-120 per minute and by pressing down one-third the depth of the anteroposterior diameter of the rib cage (chest thickness) or 4 cm in infants and 4-5 cm in children.5-7 It is best to perform chest compression by laying the patient on a flat and hard surface. For infants, the lay rescuer or a healthcare provider who is performing the CPR should use two fingers to compress the center of the chest just below the line between the nipples. For children, the rescuer should compress the lower half of the sternum with one or both hands .Special attention should be paid to avoid pressing of the xiphoid process or the rib cage. Proper depth should be maintained for each compression, 90 irrespective of whether one or both hands are used, and the chest must be allowed to recoil to its normal position after every compression. After each compression, the chest must be allowed to recoil fully, as proper venous return to the heart can be completed only when the chest is fully relaxed. During pediatric CPR, incomplete chest recoil is common, particularly when rescuers are fatigued. Incomplete chest relaxation increases pressure inside the chest cavity and reduces venous return, coronary perfusion, cardiac output, and cerebral perfusion.8, 9 Fatigue of the rescuer can lead to inadequate speed and depth of chest compression, as well as chest recoil. Even if the rescuer denies fatigue and continues CPR, the quality of chest compression will decrease within a few minutes.10, 11 If there are two or more rescuers, they should take turns to perform CPR every 2 minutes in order to prevent fatigue and reduction in the quality and speed of chest compression. The switching between the rescuers to perform chest compression should be done as soon as possible (ideally within 5 seconds) to minimize the interruption in chest compression. Each rescuer should perform 30 chest compressions and 2 ventilations, until an EMS arrives or the patient starts breathing. For CPR in infants and children, chest compression and ventilation must be provided together to yield the best outcome. CPR accompanied by both ventilation and chest compressions must be performed by a person trained in performing infant or pediatric CPR, both inside and outside the hospital. However, if a rescuer is not trained in artificial ventilation or is unable to perform it, he or she should perform chest compression until an EMS arrives.12, 13 6. Opening of the airway and ventilation As infants or children who are not responding may have their airway obstructed by their tongues, their airway must be opened by tilting the head and lifting the chin. For infants, mouth-to-mouth or mouth-to-nose breathing should be performed. Mouth-to-mouth should be used for children. While blowing the breath in, the rising of the chest should be confirmed and each breath should last for 1 second. If the chest does not rise, the head should be tilted and the mouth should be adequately covered to prevent leaking of the air before trying ventilation again. While performing ventilation for infants, if it is difficult to cover both the mouth and nose at once, mouth-to-mouth or mouth-to-nose breathing may be 91 performed. For mouth-to-mouth, the nose should be occluded, and for mouth-to-nose, the mouth should be occluded. 7. Ratio of chest compression to ventilation After performing 30 compressions, two ventilations should be performed immediately. If there is only one rescuer, 2 ventilations following 30 chest compressions should be performed, with the shortest possible break in order to minimize the duration of interruption of chest compression. When there are two rescuers, one should be in charge of chest compression and the other in charge of ventilation to sequentially perform 30 chest compressions and 2 ventilations. Chest compression and ventilation must not be performed simultaneously. Interruption of chest compression should be minimized. It would take approximately 2 minutes for one rescuer to perform 5 cycles of chest compression and ventilation at the ratio of 30:2. Two rescuers should perform chest compression and ventilation by rotating after every 5 cycles (Table 5-1). Table 5-1. Reference chart of pediatric basic life support for lay rescuers. Management Details Respiration needed CPR No respiration or only gasping (i.e., no normal breathing) Chest compression Location: the lower half of the sternum for children, just below the nipple line for infants Depth: at least one third of the AP diameter of the chest (4–5 cm for children and 4 cm for infants) Rate: 100–120/min Chest compression-to-ventilation ratio without advanced airway Chest compression-to- ventilation = 30:2 Perform compression-only CPR, if rescuers are unwilling or unable to deliver breaths Use AED Use AED as soon as it is available 92 AED analyzes rhythm Stop chest compression during rhythm analysis CPR after defibrillation Resume immediately chest compression after shock delivery Pediatric basic life support for healthcare providers PBLS for healthcare provider is essentially very similar to PBLS for the lay rescuer, except a few differences.14, 15 As healthcare providers usually work in teams rather than individually and because a series of activities is performed concurrently (for example, chest compression and preparation for ventilation), the priority of each activity is relatively less emphasized. A flow diagram of PBLS for healthcare providers is shown in Figure 5-3. 93 Figure 5-3. Algorithm of pediatric basic life support for healthcare providers. AED, automated external defibrillator; CPR, cardiopulmonary resuscitation. 1. Checking for patient response and breathing If an unresponsive patient is gasping or not breathing at all, the rescuer should understand that the patient is undergoing a cardiac arrest and requires CPR. The rescuer should lightly tap the patient and shout out “are you okay?” or call out the name of the patient if known. Then, the rescuer should promptly check whether the child has injuries or requires medical treatments. 2. Activation of the EMS 94 If a patient is neither responding nor breathing (or he/she has abnormal breathing such as gasping), the rescuer should ask nearby individuals to activate an EMS and request for an AED. 3. Checking patient pulse If an infant or a child is neither responding nor breathing normally, a healthcare provider should check for their pulse within 10 seconds. For infants, the pulse should be checked on the brachial artery, and for children, on the carotid or femoral artery. If a pulse is not detected within 10 seconds or if it is uncertain, chest compression should be started.2 1) Case of palpable pulse and inadequate breathing If a pulse is detected to be more than 60 per minute but breathing is inadequate, ventilation should be provided at the speed of 12-20 times per minute (1 breath every 3-5 seconds) until the return of spontaneous breathing. The pulse should be rechecked every 2 minutes, and each pulse check should not exceed 10 seconds. 2) Case of bradycardia and poor systemic perfusion If the pulse rate is less than 60 per minute and the perfusion status is poor (i.e., pale skin, patches of spots, or cyanosis is observed) even with oxygen and adequate ventilation, chest compression should be performed. As the cardiac output of infants and children depends greatly on the heart rate, bradycardia with poor systemic perfusion signals the necessity for chest compression. Performing CPR immediately after the occurrence of cardiac arrest can lead to an increased survival rate. Although the critical value of the heart rate at which chest compression should be performed is not yet clearly defined, chest compression is recommended for a heart rate less than 60 per minute and poor perfusion for the convenience of education and ease of memorization. 95 4. Chest compression Chest compression should be performed if infants or children do not respond, are not breathing, and do not have a pulse (or if it is unclear whether they have a pulse). The differences between a healthcare provider and a lay rescuer are in the method of chest compression in infants. When a healthcare provider is alone, chest compression using two fingers is performed for an infant. The two-thumb encircling method for chest compression is performed when there are two or more rescuers. The sides of the thorax of an infant are wrapped around with open hands, with the two thumbs side-by-side on the sternum for strong compression. The advantage of the two-thumb encircling method is that it increases perfusion pressure of the coronary artery to a greater extent compared to the two-finger chest compression, allowing pressure depth and strength consistency to generate higher systolic and diastolic blood pressures.16-18 If it is not possible to wrap the side of the thorax with both hands, the chest should be compressed using two fingers. The location for chest compression should be the lower half of the sternum in children and the sternum just below the nipple line in infants. 5. Opening of the airway and ventilation After 30 chest compressions (15 compressions in the case of two rescuers), the airway is opened using head-tilt chin-lift maneuver followed by 2 ventilations. If there are signs of spinal cord injury, head tilting should not be performed. Instead, the airway should be opened using the jaw-thrust method. As proper ventilation with an opened airway is extremely important for pediatric CPR, head-tilt chin-lift maneuver should be performed if jaw-thrust is not sufficient to open the airway. 6. Ventilation 1) Method of ventilation If it is difficult to concurrently cover the mouth and nose while performing ventilation on infants, mouth-to96 mouth or mouth-to-nose breathing may be performed. When mouth-to-mouth breathing is performed, the nose should be closed. For mouth-to-nose breathing, the mouth should be closed. In both cases, rising of the chest should be confirmed during ventilation. 2) Ventilation method to prevent hyperventilation Before establishing an advanced airway (such as endotracheal intubation, or supraglottic airway), ventilation is performed twice after 30 chest compressions (one rescuer) or 15 chest compressions (two healthcare provider rescuers), with mouth-to-mouth breathing or the bag-mask method. After establishing an advanced airway, the “compression-ventilation ratio” of CPR is not used. Chest compression at the speed of 100-120 per minute and 10 ventilations per minute are performed consistently. Two or more healthcare providers take turns in performing compression every 2 minutes to prevent the rescuers from getting fatigued. If the perfusion rhythm returns but there is no breathing, ventilation is performed 12-20 times per minute (1 ventilation every 3-5 seconds). Excessive ventilation during CPR reduced venous return, leading to decreased cardiac output and cerebral blood flow, and increases pressure within the thoracic cavity, leading to decreased coronary artery perfusion.19 Therefore, rescuers should perform ventilation by following the recommended frequency of ventilation. Because manual bag-mask ventilation can provide high pressure, ventilation is performed to the extent in which the chest rise is just observed. 3) Two-rescuer bag-mask ventilation In the case with the difficulty in attaching the mask, severe obstruction in the airway, or poor lung elasticity, bag-mask ventilation performed by two rescuers together can be useful and helpful in providing effective bagmask ventilation to the patients. One rescuer should maintain the airway and tightly seal the mask onto the face using both the hands while the other compresses the ventilation bag. Both rescuers should confirm rise of the chest. 97 4) Gastric inflation and cricoid pressure As gastric inflation may prevent effective ventilation and induce regurgitation, it should be avoided. To minimize gastric inflation, each ventilation should be performed for 1 second to prevent excessive pressure during exhalation. In addition, the application of cricoid pressure can be considered although its application is not recommended in a routine procedure. It should be considered only when the patient is unconscious and there is another healthcare provider to provide help, and it should be performed with caution as excessive cricoid pressure can block the airway. 5) Oxygen One hundred percent oxygen is provided during CPR, because there has been no report of any harmful effects of differing oxygen concentrations in humans, after the neonatal period. When the patient’s condition has stabilized, oxygen should be provided with monitoring of the saturation. The provision of humidified oxygen can prevent the drying of the mucous membrane and thickening of lung secretions. Oxygen is provided using a mask or a nasal cannula. 7. Ratio of chest compression and ventilation One rescuer performs chest compression and ventilation at the ratio of 30:2. When two rescuers perform CPR on infants or children, one performs chest compression and the other performs ventilation at the ratio of 15:2, with opening of the airway. The interruption of chest compression for the ventilation should be minimized. After intubation, the ratio of chest compression and ventilation is no longer followed. Instead, the rescuer responsible for chest compression does not stop the compression for ventilation and performs it continuously at the speed of 100-120 per minute. The rescuer responsible for ventilation provides ventilation at the speed of 10 times per minute (1 ventilation every 6 seconds). 98 8. Defibrillation VF may be the cause of sudden cardiac arrest or it may occur during CPR. The sudden collapse of child in the presence of another person (for example, a child who collapsed while exercising) that may be caused by VF or pulseless ventricular tachycardia (VT), immediate CPR and prompt defibrillation are necessary in such cases. As VF or pulseless VT may respond to defibrillation, they are categorized as “shockable rhythms”. In infants, it is better to use a manual defibrillator by well-trained healthcare provider to give a shock. For defibrillation, the first energy dose is at 2-4 J/kg and the second is 4 J/kg or higher; the shock should not exceed the maximum dose for adults.20, 21 If a manual defibrillator is not available, an AED with a pediatric energy attenuator should be used. However, if both a manual defibrillator and an AED with a pediatric energy attenuator are lacking, an AED for adults without an attenuator can be used for infants. Rescuers should minimize the time between chest compression and defibrillation, and resume CPR by restarting chest compression immediately after the defibrillation. The use of an AED will ensure that rescuers reanalyze the rhythm every 2 minutes, and defibrillation should be performed immediately after chest compression (Table 5-2). Table 5-2. Reference chart of pediatric basic life support for healthcare providers. Management Details Breathing requiring CPR Apnea or agonal breathing Check pulse and breathing Check pulse and look for no breathing or only gasping simultaneously within 10 seconds Compression Location: lower half of sternum ( for children), center of the chest, just below the nipple line (for infant) Depth: One-third AP diameter of chest (children 4–5 cm, infant 4 cm) Rate: 100–120/min Compression-to-ventilation ratio 1 rescuer: Begin cycles of 30 compressions and 2 ventilation 99 2 rescuers: Use 15:2 ratio Pulse more than 60 per minute with adequate perfusion Provide ventilation: 1 breath every 3–5 seconds or about 12–20 breaths per minutes AED analyzes rhythm Stop compression CPR after defibrillation Resume CPR immediately after defibrillation CPR, cardiopulmonary resuscitation; AP, anteroposterior; AED, automated external defibrillator 9. Compression-only CPR In infants and children, performing both chest compression and ventilation is the best CPR methods. As the most common cause of cardiac arrest in infants and children is asphyxia arrest, ventilation is required as a part of effective CPR.22 Therefore, infant and pediatric CPR accompanies resuscitation comprising ventilation and chest compression. However, if artificial ventilation is not possible or the rescuer is not known about how to perform ventilation, compression-only CPR must be performed on its own.12, 13 Resuscitation under special conditions 1. Ventilation through tracheostomy Caretakers of children with tracheostomy (parents, school nurses, or home healthcare providers) should know how to maintain the airway, clear airway discharges, and perform CPR through the artificial airway. Ventilation should be performed through tracheostomy while confirming airway maintenance and rising of the chest. If ventilation through tracheostomy is not effective even after effective suctions, maintenance of the airway should be reconfirmed. In patients who received tracheostomy, mouth-to-tracheostoma breathing is performed. When the tracheostoma is already sealed, bag-mask ventilation is performed through the nose or mouth.23 100 2. Trauma Although the criteria for performing CPR in children with injuries are the same as those in children with other diseases, some aspects should be emphasized. Errors in the opening and maintaining the airway, as well as errors due to unawareness of internal bleeding, commonly occur during pediatric resuscitation. Following are some precautions that must be taken while performing CPR on pediatric patients with injuries:24 A suction device should be used if there is a possibility of airway obstruction due to broken tooth pieces or blood. If there is external bleeding, external pressure should be applied to stop the bleeding. Considering the mechanism of injury, if there is a possibility of spinal cord injury, the movement of the cervical spine should be minimized and the head or neck should not be pulled or moved. The airway should be opened using jaw-thrust, not head-tilt. If jaw-thrust is not sufficient to maintain the airway, head-tilt chin-lift maneuver can be performed. If there are two rescuers, one opens the airway and the other prevents the movement of the cervical spine. As infants and children have relatively large heads, the best position to prevent bending of the cervical spine can be achieved by placing the back of the head on a recessed location or fixing the body in a slightly raised position.25 Children with multi-organ injuries should be transferred to a trauma center with a pediatric specialist if possible. Thoracotomy may be considered for children with penetrative injuries.26 3. Near drowning In the case of near drowning, the duration of submersion in water is an important factor for the prediction of prognosis. The age, promptness of emergency treatment, form of water (e.g., sea water), water temperature, and the presence or absence of witnesses are not reliable prognosis factors.27 As the survival rate is relatively high in the case of near drowning in ice water even with long submersion durations, the rescue time should be extended in such case.28, 29 Nearly drowned children must start receiving CPR immediately after being rescued from the water. Rescuers with special training may start ventilation in water. Because chest compression is not efficient in water, it is not usually performed.30 As there is no evidence that water causes airway obstruction, no time is wasted to pump out water from the lungs of the rescued person.31 CPR should be started by performing chest compression and the airway is opened, ventilation is performed twice. If the rescuer is alone, 5 cycles of chest 101 compression and ventilation are performed before calling EMS and preparing an AED. If there are two rescuers, one continues CPR while the other activates EMS and prepares an AED.32 102 References 1. Lopez-Herce J, Garcia C, Rodriguez-Nunez A, et al. Long-term outcome of paediatric cardiorespirato ry arrest in Spain. Resuscitation 2005;64:79-85. 2. Marsch S, Tschan F, Semmer NK, Zobrist R, Hunziker PR and Hunziker S. ABC versus CAB for cardiopulmonary resuscitation: a prospective, randomized simulator-based trial. Swiss medical weekly 20 13;143:w13856. 3. Lubrano R, Cecchetti C, Bellelli E, et al. Comparison of times of intervention during pediatric CPR maneuvers using ABC and CAB sequences: a randomized trial. Resuscitation 2012;83:1473-7. 4. Van Vleet LM and Hubble MW. Time to first compression using Medical Priority Dispatch System compression-first dispatcher-assisted cardiopulmonary resuscitation protocols. Prehospital emergency care : official journal of the National Association of EMS Physicians and the National Association of State EMS Directors 2012;16:242-50. 5. Sutton RM, French B, Niles DE, et al. 2010 American Heart Association recommended compression depths during pediatric in-hospital resuscitations are associated with survival. Resuscitation 2014;85:117 9-84. 6. Maher KO, Berg RA, Lindsey CW, Simsic J and Mahle WT. Depth of sternal compression and intr a-arterial blood pressure during CPR in infants following cardiac surgery. Resuscitation 2009;80:662-4. 7. Sutton RM, French B, Nishisaki A, et al. American Heart Association cardiopulmonary resuscitation quality targets are associated with improved arterial blood pressure during pediatric cardiac arrest. Resu scitation 2013;84:168-72. 8. Yannopoulos D, McKnite S, Aufderheide TP, et al. Effects of incomplete chest wall decompression during cardiopulmonary resuscitation on coronary and cerebral perfusion pressures in a porcine model o f cardiac arrest. Resuscitation 2005;64:363-72. 9. Zuercher M, Hilwig RW, Ranger-Moore J, et al. Leaning during chest compressions impairs cardiac 103 output and left ventricular myocardial blood flow in piglet cardiac arrest. Critical care medicine 2010;3 8:1141-6. 10. Hightower D, Thomas SH, Stone CK, Dunn K and March JA. Decay in quality of closed-chest co mpressions over time. Annals of emergency medicine 1995;26:300-3. 11. Ochoa FJ, Ramalle-Gomara E, Lisa V and Saralegui I. The effect of rescuer fatigue on the quality of chest compressions. Resuscitation 1998;37:149-52. 12. Kitamura T, Iwami T, Kawamura T, et al. Conventional and chest-compression-only cardiopulmonar y resuscitation by bystanders for children who have out-of-hospital cardiac arrests: a prospective, nation wide, population-based cohort study. Lancet (London, England) 2010;375:1347-54. 13. Goto Y, Maeda T and Goto Y. Impact of dispatcher-assisted bystander cardiopulmonary resuscitatio n on neurological outcomes in children with out-of-hospital cardiac arrests: a prospective, nationwide, p opulation-based cohort study. Journal of the American Heart Association 2014;3:e000499. 14. Berg MD, Schexnayder SM, Chameides L, et al. Part 13: pediatric basic life support: 2010 Americ an Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122:S862-75. 15. Maconochie IK, de Caen AR, Aickin R, et al. Part 6: Pediatric basic life support and pediatric ad vanced life support: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Ca rdiovascular Care Science with Treatment Recommendations. Resuscitation 2015;95:e147-68. 16. Menegazzi JJ, Auble TE, Nicklas KA, Hosack GM, Rack L and Goode JS. Two-thumb versus two -finger chest compression during CRP in a swine infant model of cardiac arrest. Annals of emergency medicine 1993;22:240-3. 17. Houri PK, Frank LR, Menegazzi JJ and Taylor R. A randomized, controlled trial of two-thumb vs two-finger chest compression in a swine infant model of cardiac arrest [see comment]. Prehospital em ergency care : official journal of the National Association of EMS Physicians and the National Associa tion of State EMS Directors 1997;1:65-7. 104 18. Whitelaw CC, Slywka B and Goldsmith LJ. Comparison of a two-finger versus two-thumb method for chest compressions by healthcare providers in an infant mechanical model. Resuscitation 2000;43:2 13-6. 19. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilation-induced hypotension during card iopulmonary resuscitation. Circulation 2004;109:1960-5. 20. Berg RA, Samson RA, Berg MD, et al. Better outcome after pediatric defibrillation dosage than ad ult dosage in a swine model of pediatric ventricular fibrillation. Journal of the American College of Ca rdiology 2005;45:786-9. 21. Rossano JW, Quan L, Kenney MA, Rea TD and Atkins DL. Energy doses for treatment of out-ofhospital pediatric ventricular fibrillation. Resuscitation 2006;70:80-9. 22. Berg RA, Hilwig RW, Kern KB, Babar I and Ewy GA. Simulated mouth-to-mouth ventilation and chest compressions (bystander cardiopulmonary resuscitation) improves outcome in a swine model of p rehospital pediatric asphyxial cardiac arrest. Critical care medicine 1999;27:1893-9. 23. Spaite DW, Conroy C, Tibbitts M, et al. Use of emergency medical services by children with spec ial health care needs. Prehospital emergency care : official journal of the National Association of EMS Physicians and the National Association of State EMS Directors 2000;4:19-23. 24. Crewdson K, Lockey D and Davies G. Outcome from paediatric cardiac arrest associated with trau ma. Resuscitation 2007;75:29-34. 25. Nypaver M and Treloar D. Neutral cervical spine positioning in children. Annals of emergency me dicine 1994;23:208-11. 26. Maconochie IK, Bingham R, Eich C, et al. European Resuscitation Council Guidelines for Resuscit ation 2015: Section 6. Paediatric life support. Resuscitation 2015;95:223-48. 27. Travers AH, Perkins GD, Berg RA, et al. Part 3: Adult Basic Life Support and Automated Extern al Defibrillation: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardio 105 vascular Care Science With Treatment Recommendations. Circulation 2015;132:S51-83. 28. Monsieurs KG, Nolan JP, Bossaert LL, et al. European Resuscitation Council Guidelines for Resus citation 2015: Section 1. Executive summary. Resuscitation 2015;95:1-80. 29. Mehta SR, Srinivasan KV, Bindra MS, Kumar MR and Lahiri AK. Near drowning in cold water. The Journal of the Association of Physicians of India 2000;48:674-6. 30. Szpilman D and Soares M. In-water resuscitation--is it worthwhile? Resuscitation 2004;63:25-31. 31. Modell JH, Idris AH, Pineda JA and Silverstein JH. Survival after prolonged submersion in freshw ater in Florida. Chest 2004;125:1948-51. 32. Graf WD, Cummings P, Quan L and Brutocao D. Predicting outcome in pediatric submersion victi ms. Annals of emergency medicine 1995;26:312-9. 106 Part 6. Pediatric Advanced Life Support Asphyxia cardiac arrest is more common among children than in adults, and pediatric cardiac arrest res ult from gradual deterioration due to respiratory failure or sepsis rather than arrhythmic or structural di sease itself.1 Approximately 5–15% of all in-hospital and out-of-hospital pediatric cardiac arrests exhibit ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) at the diagnosis.2 Approximately 25% of in-hospital cardiac arrests exhibit VF or pulseless VT, and the frequency of these patterns incr eases with age.3 Therefore, it has been suggested that each hospital organize and maintain an acute res ponse system or rapid response team to improve the treatment of in-hospital cardiac arrest.4 Basic life support considerations for pediatric advanced life support (PALS) 1. Collaborative management using a team approach It is important to build an efficient team of healthcare professionals that provides advanced life support during cardiopulmonary resuscitation (CPR). The following factors are important for these teams to eff ectively perform CPR: Chest compressions should be performed immediately after the need for CPR ha s been established, and ventilation should be performed if there is a second rescuer. Breathing is also i mportant for infants or children, and compression-ventilation CPR, rather than compression-only CPR, s hould be performed inside hospitals. Although the preparation of a ventilation device can delay effectiv e ventilation in some cases, chest compressions should be performed immediately for both infants and children. High-quality CPR is critical to successful PALS, and is defined as starting CPR within 10 s after identifying the cardiac arrest, an adequate compression rate, an adequate compression depth, compl ete recoil of the chest wall, minimal interruptions in the compressions, a sufficient chest expansion duri ng the ventilation, and the avoidance of hyperventilation. If two rescuers are performing chest compre ssions and breathing, the third rescuer (if available) should prepare a monitor and defibrillator, establish the medication route(s), and calculate the medication dosage(s). When several rescuers perform CPR, t he rescuers should clearly communicate their roles using precise and respectful expressions. 107 2. Patients on monitoring If the patient has an intra-arterial catheter, the adequacy of the compressions and the return of spontan eous circulation (ROSC) can be evaluated by observing the pressure waveform. Capnography is also us eful for evaluating the adequacy of the compressions and identifying ROSC. 3. Respiratory failure Respiratory failure is a condition that indicates inadequate oxygenation and/or ventilation, and should be suspected if the following symptoms are observed. · An increasing respiratory rate and signs of respiratory failure (e.g., nasal flaring, seesaw respira tion, and moaning sounds). · An inadequate respiratory rate and respiratory effort, thoracic movement, reduced breath sounds, or breathlessness in patients with a reduced level of consciousness. · Cyanosis while an external oxygen supply is being provided. 4. Shock Hypotension does not develop during the early phase of shock, which is also called compensated shock or normal pressure shock. Compensated shock presents as tachycardia, cool and pale extremities, a >2 s delay in the capillary refill time, a weak peripheral pulse with a maintained central pulse, and a no rmal blood pressure. If the compensation mechanism fails, it can result in hypoperfusion of the major organs, reduced consciousness, reduced urine output, metabolic acidosis, tachypnea, weak central pulse, and a change in skin color. Cardiac output is the product of heart rate and stroke volume. If the stroke volume is decreased due t o any cause, the heart rate is increased to compensate for the decrease in cardiac output. Sustained sin us tachycardia without other causes can be the first sign of shock, although bradycardia can develop af ter shock has progressed. Reductions in cardiac output and poor perfusions status can decrease the peri pheral pressure (intensity or quality), prolong the capillary refill time, and lower the skin temperature d espite a warm surrounding temperature. However, the blood vessels of the skin and muscles are inadeq uately dilated during early septic shock, and the patient may exhibit a palpable peripheral pulse and rel 108 atively high skin temperature, despite being in shock. The criteria of hypotension for infants and children during CPR are: l Full-term infants (0–28 days old): a systolic pressure of <60 mmHg. l Infants (1–12 months old): a systolic pressure of <70 mmHg. l Children (1–10 years old): a systolic pressure of less than (70 + [2 × age in years]) mmHg. l Children (>10 years old): a systolic pressure of <90 mmHg. These blood pressure criteria are below the fifth percentiles for the age-specific systolic pressures, and rarely occur in normal children. Advanced airway 1. Bag-mask ventilation Bag-mask ventilation is relatively effective and safe in cases of out-of-hospital CPR, compare to endotracheal intubation.5 Select an adequate size of mask, open the airway properly, completely attach the mask to the face, and maintain a sufficient respiratory rate and pressure to ensure that the chest rises properly. Hyperventilation can reduce blood flow to the brain and heart, as it increases intrathoracic pressure, reduces venous return, and reduces cardiac output.6 In addition, hyperventilation can cause air trapping in patients with peripheral airway collapse and barotrauma. Excessive inspiratory pressure can cause gastric inflation, which can lead to reflux of the stomach contents and pulmonary aspiration. In infants and children without an inserted advanced airway, perform two breaths after every 30 compressions (or after every 15 compressions if there are two rescuers). Stop compressions during the breathing, which should be performed for approximately 1 second per breath. Breaths should be performed every 6 seconds (10 per minute) without interruption of the compressions if an advanced airway is inserted. Perform only breathing every 3–5 seconds (12–20 per minute) if ROSC is achieved but respiration is inadequate. The ventilation rate should be increased when the patient is young. 2. Two-person bag-mask ventilation 109 Perform two-person bag-mask ventilation when there are two rescuers. This technique is especially helpful when a patient has airway collapse or low pulmonary compliance, or when the rescuer cannot completely attach the bag to the patient’s face.7 During two-person bag-mask ventilation, one rescuer holds the mask to the face while lifting the patient’s chin with both hands, while the other rescuer compresses the bag. Both rescuers should frequently confirm that the patient’s chest is expanding properly. 3. Endotracheal intubation Significant training is needed to successfully perform endotracheal intubation in infants and children, because they have a unique tracheal structure. Compared to adults, children’s tongues are relatively large, their airways are more flexible, the tip of their epiglottis is located at a relatively high and anterior part of the neck, and their airway is smaller. 1) Size of the pediatric endotracheal tube (ETT) Among children who weight <35 kg, even with a relatively short stature, determining the ETT’s size based on height is more accurate than using their age (e.g., using a Broselow resuscitation tape).8, 9 However, also prepare tubes that are 0.5 mm larger and smaller in internal diameter (ID) than the calculated tube size, regardless of the presence or absence of a cuff. If resistance is felt during the intubation, use the 0.5 mm smaller tube. If there is significant leakage at the glottis, the 0.5 mm larger tube or a cuffed tube should be used. For an un-cuffed tube, use a tube with an ID of 3.5 mm for infants who are <1 year old, and a 4.0-mm tube for children who are 1–2 years old. For children who are >2 years old, use the following formula: ID of the un-cuffed tube (in mm) = 4 + (age in years / 4). If a cuffed tube must be used in an emergency, use a tube with an ID of 3.0 mm for children who are <1 year old, and a 3.5 mm tube for children who are 1–2 years old. For children who are >2 years old, use the following formula10-13: ID of the cuffed tube (in mm) = 3.5 + (age in years / 4). 2) Cuffed ETT 110 Both cuffed and un-cuffed tubes can be used for endotracheal intubation in infants and children. If a cuffed tube is used during surgery, the frequency of reintubation can be reduced without an increased risk of complications.10 Using a cuffed tube in the intensive care unit (ICU) can reduce the risk of aspiration.14 If a cuffed tube is used, the cuff’s pressure should be constantly monitored and the manufacturer’s recommended pressure should be maintained (usually <20–25 cmH2O). A cuffed tube can be more effective if it is selected based on the size, location, and pressure of the cuff in cases with low pulmonary compliance, high airway resistance, or significant air leakage at the glottic area.15, 16 3) Endotracheal intubation Prepare a suction catheter, bag-mask, oxygen, and stylet before the intubation. The tip of the stylet should not pass the tip of the tube. Applying a water-based lubricant or sterile distilled water to the tip of the stylet may make it easier to remove after the intubation. Also prepare a functioning laryngoscope handle, blades, an extra light bulb, extra batteries, capnometry, tape to fix the tube, and gauze to clean the patient’s face. Perform endotracheal intubation after oxygen administration unless the patient is in cardiac arrest. Assist ventilation can be performed if the patient’s respiratory effort is insufficient. It should be performed with the preparation of a secondary method for maintaining the airway, in anticipation of intubation failure. Immobilize the cervical vertebrae to prevent spinal injury during the intubation in cases that involve severe trauma to the head, neck, or other areas. The procedure time should not exceed 30 seconds, as hypoxia or ischemic injury can occur due to inadequate or delayed intubation. Monitor the patient’s heart rate and oxygen saturation (using pulse oximetry) while performing endotracheal intubation. Stop the procedure and wait until the patient’s condition improves, while providing oxygen using a bag-mask, if the patient develops bradycardia (<60/min), a change in skin color or blood circulation status, or oxygen saturation below the normal level. In cases of pediatric cardiac arrest, the endotracheal intubation should not be delayed to set up pulse oximetry, which cannot function properly if the pulse is not palpable. Use either straight or curved laryngoscope blades. Once the tip of a straight blade passes the epiglottis, place it on the entrance of the vocal cords, lift the base of the tongue, and drag the blade anteriorly to lift the epiglottis. 111 If a curved blade is used, anteriorly adjust the location of the tongue’s base after the tip of the blade is placed in the epiglottic vallecula. At that point, the laryngoscope blade or handle should not be used as a lever, and direct pressure on the lips or gum should be avoided. The glottis entrance should be exposed for ideal endotracheal intubation. To simplify the intubation in infants and children, align the pharynx by placing a pillow under the patient’s head with the chin in the sniffing position. For infants or children who are <2 years old, it is acceptable to lay them flat without a pillow to perform intubation through the mouth. The depth of the ETT intubation can be calculated using the following formula: intubation depth (in cm) = the tube’s ID (in mm) × 3. For children who are >2 years old, the formula is: intubation depth (in cm) = (the child’s age in years / 2) + 12. 4) Checking the tube’s location The correct location of the tube cannot be verified using only clinical signs such as chest wall movement or vapor inside the tube. The tube’s location should be checked immediately after intubation, re-fixing the tube, transfer, and patient movement. The signs of a correct tube location are: · Movement of the bilateral chest wall and symmetrical breathing sounds in both lungs, and particularly in the axillary areas. · The absence of gastric inflation sounds. · Appropriate end-tidal CO2 (ETCO2). · Adequate oxygen saturation while perfusion is maintained. However, oxygen saturation can be maintained for approximately 3 minutes after hyperoxygenation despite poor ventilation. · Laryngoscopic evidence that the tube is placed between the vocal cords. · Chest radiography findings that confirm the tube is correctly located. For immobilization of tube, the tube should fixed in a neutral position to prevent the tube from sliding deeper if 112 the patient’s neck bends, or sliding out if the patient’s neck stretches.17 If the patient’s condition suddenly deteriorates while they are intubated, determine whether the tube is displaced or occluded, pneumothorax is present, or a mechanical error has occurred. 5) Capnometry or capnography If possible, verify the location of the ETT using capnometry for all age groups and in all circumstances, including in the pre-hospital, emergency room, ICU, ward, operation room, or transfer settings.16-18 However, this method cannot detect whether a tube is placed in the right main bronchus, despite the appearance of color changes or the proper waveform. Because ETCO2 may not be detected during cardiac arrest, even if the tube is properly located, the tube’s location must be checked using a laryngoscope. · If the capnometry is contaminated by gastric contents or an acidic drug, the color persists as the acidic color and does not accurately reflect the ventilation. · When epinephrine is intravenously infused, pulmonary perfusion is temporarily reduced and the ETCO2 value can decrease below the critical value.18 · If there is severe airway occlusion, such as moderate asthma or pulmonary edema, the exhalation of CO2 can decrease below the critical value.19 · In cases with air leakage at the glottis region, the CO2 is diluted and may not be detected, due to the insufficient ventilation. Drugs that are used for PALS (Table 6-1) Table 6-1. Drugs used in pediatric advanced life support Medication Dose Remarks Adenosine 0.1 mg/kg (maximum 6 mg) Monitor ECG 113 Rapid IV/IO bolus with flush Amiodarone 5 mg/kg IV/IO; may repeat twice up to 15 mg/kg Monitor ECG and blood pressure; adjust administration rate to urgency (IV push during cardiac arrest, more slowly over 20–60 min with perfusing rhythm). Expert consultation strongly recommended prior to use when patient has a perfusing rhythm. Use caution when administering with other drugs that prolong QT (obtain expert consultation) Maximum single dose 300 mg Atropine 0.02 mg/kg IV/IO Higher doses may be used with organophosphate 0.04–0.06 mg/kg ET (flush with 5 poisoning mL of normal saline and follow with 5 ventilations.) Maximum single dose: 0.5 mg Calcium chloride (10%) 20 mg/kg IV/IO, Maximum dose 2 g Administer slowly Epinephrine 0.01 mg/kg (0.1 mL/kg 1:10,000) IV/IO May repeat every 3–5 minutes 0.1 mg/kg (0.1 mL/kg 1:1000) ET (Flush with 5 mL of normal saline and follow with 5 ventilations.) Maximum dose 1 mg IV/IO; 2.5 mg ET Glucose 0.5–1 g/kg IV/IO Newborn: 5–10 ml/kg D10W Infants and children: 2–4 ml/kg D25W Adolescents: 1–2 ml/kg D50W Lidocaine Bolus: 1 mg/kg IV/IO 114 Infusion: 20–50 mcg/kg/min Magnesium sulfate 25–50 mg/kg IV/IO over 10–20 min, faster in torsades de pointes Maximum dose 2 g Sodium bicarbonate 1 mEq/kg per dose IV/IO slowly After adequate ventilation ECG, electrocardiography; IV, intravenous; IO, intraosseous; ET, endotracheal; D10W, 10% dextrose; D25W, 25% dextrose; D50W, 50% dextrose 115 1. Adenosine Adenosine temporarily blocks atrioventricular (AV) node conduction and interrupts the re-entrant mechanism. The half-life of adenosine is very short, which gives it a broad safety range. Large doses should be administered through a peripheral vein, rather than a central vein, although adenosine can be also administered intraosseously. Additional normal saline should be provided immediately after an intravenous (IV) infusion of adenosine to help the adenosine rapidly enter the central circulation. 2. Amiodarone Amiodarone delays conduction in the AV node, prolongs the refractory period and QT interval, and slows ventricular conduction. However, amiodarone should be infused as slowly as the patient’s condition allows, and their blood pressure should be monitored. The appropriate infusion rate is relatively slow if there is a pulse, and is relatively fast in cases of cardiac arrest or VF. Hypotension can develop due to vasodilation during the administration, and its magnitude is related to the administration rate, although it is less frequent when amiodarone is administered as a liquid form.20 An electrocardiogram (ECG) should be used to monitor for administration-related complications, such as bradycardia, AV block, and torsades de pointes. Special care should be taken during the coadministration of other medications that can prolong the QT interval. The half-life of amiodarone can reach 40 days, and any related adverse effect(s) may have a prolonged duration. 3. Atropine As a parasympathetolytic agent, atropine increases cardiac rhythm and AV conduction. Atropine is administered as an IV or intraosseous (IO) infusion, with no minimum dose, in pediatric cases with a risk of severe bradycardia during emergency endotracheal intubation. However, routine atropine administration is not recommended for infants and children if emergency endotracheal intubation is necessary.21-23 Large doses of atropine should be administered in cases of nerve gas poisoning or organophosphate poisoning.24 116 4. Calcium The routine administration of calcium during cardiac arrest does not improve the patient’s prognosis,3, 25, 26 and routine administration is not recommended as life support for patients who are in asystole. Calcium is used to treat proven hypocalcemia or hyperkalemia, especially in patients with hemodynamic dysfunction. A decrease in the levels of ionized calcium is relatively common in severely ill children, and especially in children with sepsis. Calcium should be considered for treating hypermagnesemia or overdose with a calcium channel blocker. The most common formation of calcium for children is 10% calcium chloride, as it has a higher bioavailability than calcium gluconate,27, 28 and this solution should be infused through a central vein due to the risk of peripheral vein injury. An IV infusion of calcium should be administered every 10–20 seconds for patients in cardiac arrest and every 5–10 minutes for patients with a perfusing rhythm. 5. Epinephrine Epinephrine is an intrinsic catecholamine that strongly stimulates the alpha and beta adrenergic receptors of the sympathetic nerves. Epinephrine’s most significant pharmacological action during cardiac arrest is vasoconstriction due to activation of alpha adrenergic receptors. This increases the aortic diastolic pressure and the perfusion pressure in the coronary artery, which is a significant determinant of successful CPR.29, 30 During compressions, the increased perfusion pressure in the coronary artery increases the oxygen supply to the heart. Epinephrine also improves the rate of successful defibrillation by increasing the VF amplitude and myocardial contraction, which stimulates spontaneous contraction. The most common rhythms during pediatric cardiac arrest are asystole and bradycardia, and epinephrine can provide a perfusing rhythm in these patients. The epinephrine can be administered using an IV/IO infusion, or through ETT in pediatric patients with symptomatic bradycardia who do not respond to effective assisted ventilation or oxygen supply. However, it is important to monitor the oxygen supply and circulation, because catecholamine activity can be reduced by acidosis or hypoxia. If the initial dose of epinephrine is not effective, it should be repeatedly administered every 3–5 minutes during CPR. 117 Although epinephrine can be absorbed when it is administered using an ETT, the absorbed amount and serum concentration cannot be predicted. Therefore, a continuous IV infusion of epinephrine can be helpful once ROSC is achieved. Epinephrine’s hemodynamic effects are related to its dosage, with low doses (<0.3 μg/kg/min) prominently resulting in beta adrenergic activity and higher doses (>0.3 μg/kg/min) predominantly causing vasoconstriction due to both beta and alpha adrenergic activities. It is preferable to administer epinephrine via the central circulation, as extravasation of epinephrine can lead to local ischemia, tissue damage, and necrosis. Similar to other catecholamines, epinephrine is inactivated in alkali solutions and should not be mixed with sodium bicarbonate. Epinephrine can be administered during CPR for infants and children who are in cardiac arrest, although there is insufficient evidence regarding the effects of other vasopressors.31-34 6. Glucose Infants have low stored levels of glucose, and a high demand for glucose. Furthermore, infants can readily develop hypoglycemia if they have a condition that requires an increased energy supply (e.g., shock). Therefore, glucose levels should be closely monitored using a rapid bedside test in cases of coma, shock, or respiratory failure. Once hypoglycemia has been confirmed, it should be treated using a glucose-containing fluid.35 Two to four milliliters of 25% glucose solution (250 mg/mL) per kilogram provides 0.5–1.0 g/kg of glucose, and 5–10 mL of a 10% glucose solution (100 mg/mL) also provides a similar amount of glucose. It is preferable to treat hypoglycemia using a continuous infusion of a glucose solution, as osmotic diuresis can be caused by a sudden increase in the plasma oncotic pressure after a single administration of a hypertonic glucose solution. The current recommendation is to maintain euglycemia during the CPR and to prevent hypoglycemia after the CPR, as there are no data regarding whether hyperglycemia is advantageous or harmful after cardiac arrest. 7. Lidocaine Lidocaine reduces myocardial autonomy and prevents ventricular arrhythmia. But it can depress the myocardium, reduces circulation, causing drowsiness, disorientation, muscle twitching, and seizure. Amiodarone and lidocaine can be used in infants and children with VF and pulseless VT that does not respond 118 to defibrilaltion.22, 36, 37 Nevertheless, there is a significant possibility of adverse effect(s) in cases with a low cardiac output, abnormal hepatic function, or abnormal renal function.38, 39 8. Magnesium Magnesium is only administered to patients with proven hypomagnesemia and torsade de pointes.40-42 A rapid IV infusion (for a few minutes) of magnesium sulfate is recommended for torsade de pointes, regardless of its cause. Magnesium causes vasodilation, and hypotension can develop when it is rapidly infused. 9. Sodium bicarbonate In most studies, the routine administration of sodium bicarbonate has not improved the post-arrest prognosis.43, 44 Adequate ventilation, oxygen supply, and effective recovery of systemic perfusion (to correct tissue ischemia) should be the primary concerns in pediatric cardiac arrest, because respiratory failure is an important cause in these cases. Once effective ventilation has been confirmed, and epinephrine with compressions has been started to maximize circulation, the administration of sodium bicarbonate can be considered in cases of a prolonged cardiac arrest. Sodium bicarbonate is also recommended for patients with symptomatic hyperkalemia, hypermagnesemia, and overdose with tricyclic antidepressants or other sodium channel blockers. If indicated, sodium bicarbonate is administered as an IV or IO infusion, and a diluted solution can be used to prevent increased oncotic pressure in neonates, although there is no evidence that a diluted solution is beneficial in infants or children. The appropriate dose of sodium bicarbonate can be determined using blood gas analysis. Because catecholamine is inactivated by sodium bicarbonate, and calcium forms a precipitate when it is mixed with sodium bicarbonate, 5–10 mL of normal saline should be used to wash the IV line after administering sodium bicarbonate. 10. Vasopressin 119 Vasopressin is an intrinsic hormone that activates a specific receptor and mediates systemic vasoconstriction or water reabsorption in renal tubules. There is insufficient data to determine whether the routine use of vasopressin can be recommended in cases of pediatric cardiac arrest. Vasopressin or terlipressin (a long-acting drug) can be effective in children or adults who have failed standard treatment for cardiac arrest.45-47 Treatment for pulseless arrest (Figure 6-1) Figure 6-1. Algorithm of pediatric cardiac arrest. CPR, cardiopulmonary resuscitation; VF, ventricular fibrillation; VT, ventricular tachycardia; PEA, pulseless electrical activity; IO, intraosseous; IV, intravenous; ROSC, return of spontaneous circulation If a child is unresponsive and breathless, the responder should immediately start high-quality CPR, supply oxygen (if possible), and ask someone to bring a defibrillator. An ECG monitor or automated external 120 defibrillator (AED) electrodes should be attached as soon as possible. Cardiac rhythm is monitored using an ECG monitor during CPR for children, although an AED will automatically notify the rescuer if the patient has a shockable rhythm (VF or pulseless VT) or a non-shockable rhythm (asystole or pulseless electrical activity [PEA]). Temporarily interrupting the compressions may be necessary to check the rhythm. Asystole or wide QRS bradycardia is the most common rhythms during asphyxial cardiac arrest. Although VF or PEA does not frequently occur in infants or children, there is a high probability of VF-induced cardiac arrest in cases of sudden witnessed cardiac arrest among older children. 1. Non-shockable rhythm (asystole/PEA) The definition of PEA is the presence of organized electrical activity, such as a slow and wide QRS, without a palpable pulse. There can be a normal heart rate without a pulse and with poor tissue perfusion during the early stage of suddenly impaired cardiac output. This condition is more reversible than asystole and used to be known as electromechanical dissociation. Minimize any interruption in the compressions and continue CPR. The second rescuer should establish an IV line and administer epinephrine at 0.01 mg/kg (0.1 mL/kg in a 1:10,000 solution) during the CPR, and the same dose should administered every 3–5 minutes. High-dose epinephrine does not improve the survival rate, and can cause harm, although it may be considered in exceptional cases, such as cases of overdose with beta blockers.32, 48 If an advanced airway has been placed, the first rescuer should perform constant compressions at a rate of ≥100– 120 per minute, and the second rescuer should provide breaths every 6 seconds (approximately 10 per minute). The rescuer(s) who are performing the compressions should switch approximately every 2 minutes, while minimizing the interruption, to provide optimal compression quality and speed, and to avoid compressioninduced fatigue. During this period, the rhythm should be monitored while minimizing any interruption of the compressions. If the rhythm is non-shockable, CPR should be continued with epinephrine administration until there is evidence of ROSC or a decision is made to cease CPR. If the rhythm changes to a shockable rhythm, immediate compressions and defibrillation should always be performed, and the rhythm should be rechecked 121 after 2 minutes of CPR. The period between stopping or restarting the compressions and the defibrillation should be minimized. Find reversible cause(s) and correct them. 2. Shockable rhythm (VF/pulseless VT) Defibrillation is the most important treatment for VF, and provides an overall survival rate of approximately 17– 20%.49 The resulting survival rate is higher for primary VF, compared to secondary VF, and the survival rate after adult cardiac arrest decreases by 7–10% for every 1-minute delay in starting CPR and defibrillation.50 The survival rate is highest when high-quality CPR is performed with minimal interruptions during the early stage of cardiac arrest. The output of defibrillation is better when the rescuer minimizes the time between the compressions and defibrillation. Defibrillator As AEDs can detect the pediatric heart rhythm, they should be installed in facilities that treat children with a risk of arrhythmia or cardiac arrest. The ideal defibrillator can adjust the energy dose for children. 1. Electrode size A manual defibrillator typically has different sizes of electrodes for adults and children, and some manual defibrillators have self-adhesive electrodes. In pediatric cases, the largest appropriate electrode should be selected based on the patient’s chest size. The electrodes should not contact each other, and the space between the two electrodes should ≥3 cm. Self-adhesive electrodes should be completely attached to the patient’s chest by firmly pressing them onto the chest. The adult size of electrodes (8–10 cm) is used for children who are ≥1 year old or weigh >10 kg, and the pediatric size is used for infants who are <1 year old or weigh <10 kg. 122 2. Interface Self-adhesive electrodes have pre-spread electrode gel on the interface that should be placed on the patient’s chest. However, electrode gel must be applied for manual electrodes. Normal saline, ultrasound gel, or alcohol are not appropriate replacements for electrode gel. 3. Electrode placement The manufacture’s recommendations should be followed when placing a self-adhesive AED or monitor/defibrillator. Manual electrodes are placed at the apex (at the left lower rib, lateral to the left nipple) and the right upper quadrant of the chest, which locates the heart between the electrodes. The electrodes must be firmly applied to maintain a strong contact, and there is no benefit to placing the electrodes on the anterior and posterior sides of the patient’s trunk. 4. Energy dose The lowest energy dose for effective defibrillation and the upper limit for safe defibrillation in infants or children are unknown. The first recommended energy dose is 2–4 J/kg for monophasic or biphasic defibrillators if the infant or child exhibits VF or pulseless VT. The second recommended dose is 4 J/kg, and any subsequent dose should never exceed the maximum adult dose. If there is no exact energy dose meter on the defibrillator, use the next highest energy on the energy selector when escalating the dose.51-53 5. AED VF can be accurately detected by most AEDs in children of all ages. If the AED does not have an energy attenuating device, a manual defibrillator is preferred for children who are <1 year old. An AED with an energy attenuating device can be used unless a manual defibrillator is available. If both an AED with an energy attenuating device and a manual defibrillator are unavailable, an AED without an energy attenuating device can 123 be used in children. 6. Integrating defibrillation and CPR CPR should be performed until the defibrillator is prepared and defibrillation is feasible, and the compressions should be re-started immediately after the defibrillation. It is ideal to only interrupt the compressions for checking cardiac rhythm, performing defibrillation, and breathing before placing an advanced airway. Once the rhythm has been evaluated, start and continue the compressions until the defibrillator is charged, even in cases with a shockable rhythm.The first defibrillation (2–4 J/kg) should be started as soon as possible, and CPR with compressions should be immediately re-started after the defibrillation. It is very important to minimize the interval between starting or stopping the compressions and the defibrillation. Continue CPR for approximately 2 minutes, although this sequence may be changed based on an expert’s opinion if the environment can facilitate continuous invasive monitoring (e.g., in a hospital). An IV or IO line can be established if there are enough rescuers. Rhythm should be checked after 2 minutes of CPR, and the defibrillator should be charged at 4 J/kg. If a shockable rhythm persists, defibrillation should applies at 4 J/kg, and the algorithm for asystole/PEA should be followed in a non-shockable rhythm is observed.(5) Resume the compressions immediately after the second defibrillation, and continue CPR for approximately 2 minutes. Epinephrine should be administered at 0.01 mg/kg (0.1 mL/kg in a 1:10,000 solution) every 3–5 minutes during the CPR. If there is a third rescuer, epinephrine should be prepared and administered as soon as possible, and before checking the rhythm. The rescuer who is in charge of the defibrillator should prepare the third defibrillator charge before checking the ECG rhythm (>4 J/kg and <10 J/kg or the maximum adult dose). If there is a shockable rhythm, an additional defibrillation should be administered (>4 J/kg and <10 J/kg or the maximum adult dose), and CPR should be immediately resumed. If the defibrillation is unsuccessful, amiodarone or lidocaine should be administered while continuing the CPR. The algorithm for pulseless cardiac arrest is always followed if there is a nonshockable rhythm. If an advanced airway is placed, one rescuer should continue compressions at a rate of ≥100– 120 per minute, and the second rescuer should perform breathing every 6 seconds (10 per minute). If there are 124 two or more rescuers, they should switch every 2 minutes to prevent compression-induced fatigue and to maintain adequate compression speed and quality. If there is an organized rhythm at 2 minutes after the defibrillation, check the pulse to determine whether it is a perfusing rhythm. ROSC is predicted if the ETCO2 rapidly increases during the compressions or the monitored arterial waveform increases. If both ROSC and a pulse are achieved, post-CPR management can be started. However, if VF re-develops after the successful defibrillation, CPR should be re-started and defibrillations should be attempted with the dose which achieves successful defibrillation. Find and correct any other reversible causes. Management of torsade de pointes Torsade de pointes is polymorphic VT and is associated with a prolonged QT interval. A prolonged QT interval can develop due to congenital conditions or drug toxicity, and is associated with class 1A antiarrhythmic drugs (procainamide, quinidine, and disopyramide), class III antiarrhythmic drugs (sotalol and amiodarone), tricyclic antidepressants, digoxin, and drug interactions.54, 55 Torsade de pointes typically progresses to VF or pulseless VT. Therefore, if pulseless cardiac arrest develops, the rescuer must start CPR and perform defibrillation. Regardless of the cause, magnesium (at 25–50 mg/kg to a maximum dose of 2 g) should be rapidly administered for a few minutes as an IV infusion. Post-CPR management Post-CPR management should begin immediately after ROSC in patients who had shock, respiratory failure, and cardiac arrest. The purposes of post-CPR management are to: 1) maintain brain function, 2) avoid secondary organ damage, 3) correct the cause(s) of the cardiac arrest, and 4) prepare for the next treatment step with an optimal hemodynamic status. Because the patient’s condition can deteriorate after a short period of temporary stabilization, the patient should be frequently monitored. Thoroughly determine whether the airway is secure, oxygen is supplied, and ventilation and perfusion are stabilized. Look for evidence of trauma and reevaluate the patient’s neurological condition during the examination. Check for any history of allergy, disease, medication, or vaccination, and evaluate the patient’s renal and hepatic functions (dysfunction can indirectly affect the 125 patient’s prognosis). 1. Management of the respiratory system After children have received CPR, oxygen should be supplied until adequate oxygenation and proper oxygen carrying capacity is achieved, as measured using pulse oximetry or direct arterial blood gas analysis. High-dose oxygen should be administered if there are symptoms of significant respiratory distress (e.g., anxiety, breathing impairment, cyanosis, or hypoxemia), and endotracheal intubation with mechanical ventilation can be performed. If the intubated patient experiences a sudden deterioration, consider the possibility of displacement or obstruction of the ETT, pneumothorax, or mechanical errors. Analgesics or sedatives can be used for anxious patients if these factors are confirmed to be absent. However, careful attention is warranted, as seizure can be masked by the use of a neuromuscular blocker. A target arterial CO2 partial pressure can be established and maintained based on the patient’s specific condition after ROSC is achieved. There is no evidence that hypercapnia or hypocapnia are more beneficial than eucapnia for improving the patient’s survival rate and quality of life.56, 57 Oxygen should be supplied to provide proper oxygenation for intubated patients, and the respiratory rate should be maintained at 30–40/min for infants and 20–30/min for children. A sufficient tidal volume will cause the chest to visibly rise. Once mechanical ventilation is started, the early tidal volume should be maintained at 6 mL/kg, which should cause the chest to visibly rise and yield respiratory sounds at the periphery of the lung that can be detected using auscultation. A value of approximately 3–6 cmH2O should be used for positive end-expiratory pressure, although a higher value can be used if the functional residual volume is reduced and the lung has collapsed. Arterial blood gas analysis should be performed at 10–15 minutes after early mechanical ventilation, and it is recommended that normal arterial oxygen partial pressure be maintained unless there is a specific reason for deviation.56, 58, 59 Cardiac anomalies in children should be evaluated via echocardiography immediately after CPR, as the proper oxygen saturation can vary based on the patient’s hemodynamic status and congenital heart disease(s). Nasogastric or orogastric tube insertion is needed, as gastric inflation can cause discomfort and ventilation impairment. 126 2. Cardiovascular management Because circulatory failure can develop after recovery from cardiac arrest, continuous or frequent evaluation of the cardiovascular system should be performed to rapidly detection of any decreased cardiac output or the development of shock. Inadequate tissue perfusion can result in a prolonged capillary refill time, a reduced or absent peripheral pulse, a change in consciousness, cold extremities, tachycardia, a decreased urine output, and hypotension. An insufficient supply of fluid after CPR can cause a reduction in the cardiac output or shock that develops secondary to the reduced peripheral vascular resistance and myocardial stunning.60 Heart rate, blood pressure, and oxygen saturation should be constantly monitored after CPR, and blood pressure should be monitored using an intra-arterial catheter (if possible) in patients with cardiovascular dysfunction. Because hypotension can frequently occur during the period of ROSC after CPR, and this condition is associated with a poor prognosis, the systolic pressure should be maintained at or above the fifth age-specific percentile, and IV fluids or inotropic agents should be administered.61-63 Urine output is a significant indicator of internal organ perfusion, and should be monitored using a urine catheter in patients with hemodynamic dysfunction. The IO route should be removed once a secure IV line is established. 3. Drugs to maintain cardiac output Myocardial impairment and vascular instability frequently occur after recovery from cardiac arrest. After CPR, systemic and pulmonary vascular resistance usually increases during the early phase, except in cases of septic shock. Cardiovascular function also constantly changes after CPR, as it exhibits a hyperdynamic status during the early phase, which subsides towards a gradual weakening of cardiac function. Therefore, if abnormal cardiovascular function is observed or suspected after CPR, an adequate dose of vasoactive drug(s) should be administered to improve cardiac function and tissue perfusion. The selection and dose of the drug(s) should be based on the individual patient’s status, and should be administered using an accurate IV route. 127 1) Epinephrine Epinephrine is used to treat shock for any reason, which does not respond to fluid administration and exhibits extremely low systemic perfusion. As a strong vasoconstrictor, epinephrine increases systemic vascular resistance and heart rate through its chronotropic activity. Epinephrine can be administered during bradycardia with hemodynamic changes that do not respond to oxygen and mechanical ventilation. Low-dose epinephrine (<0.3 μg/kg/min) works as a strong inotropic agent and reduces systemic vascular resistance by activating beta adrenergic receptors. If the dose is increased to >0.3 μg/kg/min, epinephrine exerts both an inotropic effect and increases systemic vascular resistance by activating the vascular alpha adrenergic receptors. As epinephrine’s effects vary according to the dose in different patients, the dose must be frequently adjusted to achieve its intended effect. Epinephrine is more effective than dopamine in patients with severe circulatory compromise, and especially in infants.64 2) Dopamine Dopamine has beta and alpha sympathomimetic effects through a direct dopaminergic effect and an indirect stimulatory effect on norepinephrine secretion. The dose of dopamine must be frequently adjusted when it is used to treat shock with low systemic vascular resistance and no response to fluid administration. Although it barely affects the systemic hemodynamic status at low doses (0.5–2 μg/kg/min), dopamine typically increases the blood flow to the heart and intestine, and increases cardiac output and blood pressure in neonates.65 At doses of >5 μg/kg/min, dopamine induces cardiac beta adrenergic receptor activity, which induces the secretion of norepinephrine from the cardiac sympathetic nerve. However, dopamine’s ability to stimulate myocardial and vascular contraction can be reduced, as myocardial norepinephrine is depleted in patients with chronic cardiac failure, and the development of the cardiac sympathetic nerve is incomplete in infants who are <1 month old. At doses of >20 μg/kg/min, dopamine induces excessive vasoconstriction and renovascular dilatation disappears. Therefore, epinephrine or dobutamine are recommended in cases where >20 μg/kg/min of dopamine would be needed to increase myocardial contraction. Dopamine is a catecholamine that can be partially inactivated in alkali solutions, and should not be mixed with bicarbonate.66 128 3) Dobutamine Dobutamine is a synthetic catecholamine that exerts relatively selective effects on the beta-1 adrenergic receptor, and has minimal effects on the beta-2 adrenergic receptor. Therefore, dobutamine is a relatively selective inotrope that can increase myocardial contraction and reduce systemic vascular resistance.67 Dobutamine is effective for increasing cardiac output and blood pressure in infants and children. In particular, dobutamine can be used to treat secondary reductions in cardiac output due to decreased myocardial function, such as in the post-cardiac arrest condition. Tachycardia and premature ventricular contraction can occur at high doses of dobutamine. 4) Norepinephrine Norepinephrine is a neurotransmitter that is secreted from the sympathetic nerve, and is a strong inotrope that it works on the peripheral alpha and beta sympathetic nerves to induce strong myocardial and peripheral vascular contractions. The alpha sympathomimetic effect is predominant at the standard dose. As norepinephrine is a strong vasoconstrictor, it can be used to treat septic shock that does not respond to fluid infusion and exhibits low systemic vascular resistance, spinal shock, and anaphylaxis. The infusion rate may be adjusted according to the patient’s blood pressure and perfusion status. 5) Nitroprusside Nitroprusside is a vasodilator that induces the local production of nitric oxide in all blood vessels. At the therapeutic dose, it has no direct effects on myocytes, and increases cardiac output by reducing the resistance of the systemic and pulmonary blood vessels. The combination of nitroprusside and inotropes can be used in patients with severe hypertension or reduced cardiac output due to reduced myocardial function and increased vascular resistance. However, it should not be used if the blood volume is reduced, as it can cause severe hypotension. Nitroprusside is rapidly metabolized and should be constantly infused with a dextrose solution, and 129 should not be mixed with normal saline. Levels of thiocyanate should be monitored in cases with prolonged use, and especially when the infusion rate is >2 μg/kg/min. 6) Inodilators Inodilators, such as amrinone and milrinone, are used for patients with reduced cardiac function or increased resistance of the systemic and pulmonary blood vessels. Similar to vasodilators, inodilators do not increase the myocardial oxygen demand, increase the cardiac output, and have minimal effect on the heart rate. Hypotension is not common if the circulating blood volume is adequate, but can occur due to vasodilation if there is an inadequate circulating blood volume. Therefore, fluid administration may be necessary to counteract vasodilation after drug administration.68 4. Nervous system management The primary purpose of CPR is to maintain brain function, and care must be taken to prevent secondary damage to the nervous system after CPR. Hyperventilation has a negative effect on the prognosis of the nervous system, as it affects both cardiac function and cerebral perfusion. Short periods of intentional hyperventilation are acceptable in cases with signs of brain hernia, such as a sudden increase in intracranial pressure, mydriasis without a light reflex, bradycardia, or hypertension. Target temperature management can be considered for unconscious infants or children with ROSC after cardiac arrest. The body temperature should not be allowed to drop below 32°C, or to increase above 37.5°C, even if target temperature management is not performed.69-74 As fever has a negative effect on the recovery of brain function, it should be actively treated using an antipyretic drug and an external cooling method. Tremors can occur at low temperatures, and can be prevented using a sedative. A neuromuscular blockade can be used if necessary, although it can mask a seizure, and continuous electroencephalogram monitoring can be used to detect seizures.75 Although an adequate cooling and rewarming method has not been established, the body temperature should not increase at a rate of >0.5°C every 2 hours, unless there is another reason for rapid rewarming. 130 5. Renal system management The prerenal condition that is caused by dehydration or inadequate perfusion, and/or ischemic injuries in the kidney(s), can reduce urine output (infants and children: <1 mL/kg/h, adolescents: <30 mL/h). Avoid using drugs with renal toxicity until the patient’s renal function has been confirmed, and adjust the dose of drugs that undergo renal excretion. 6. Gastrointestinal system management In cases with no bowel sounds, abdominal distention, or required mechanical ventilation, perform nasogastric or orogastric intubation to prevent or treat gastric inflation. However, nasogastric intubation is prohibited in patients with facial injuries or basal skull fractures, because the tube can enter the cranium. 7. Factors predicting prognosis The survival rate is higher in cases with a pupillary reflex at <24 hours after CPR, compared to that in cases that do not fulfill this criterion,3, 76-79 and there are reports that a poor prognosis may be predicted by increased levels of neuron-specific enolase (NSE) and S100 calcium-binding protein B (S100B).77, 80, 81 Although there are no established predictors of neurological and survival outcomes in children with ROSC, these outcomes may be predicted by pupillary reflex, NSE and S100B levels. Furthermore, electroencephalogram results at <7 days after cardiac arrest may help predict neurologic outcomes,75, 79 although these outcomes cannot be predicted using only electroencephalogram results. 131 References 1. Kuisma M, Suominen P, Korpela R. Paediatric out-of-hospital cardiac arrests--epidemiology and outcome. Resuscitation 1995; 30: 141-50. 2. Donoghue AJ, Nadkarni V, Berg RA, et al. Out-of-hospital pediatric cardiac arrest: an epidemiologic review and assessment of current knowledge. Ann Emerg Med 2005; 46: 512-22. 3. Meert KL, Donaldson A, Nadkarni V, et al. Multicenter cohort study of in-hospital pediatric cardiac arrest. Pediatr Crit Care Med 2009; 10: 544-53. 4. Tibballs J, Kinney S. Reduction of hospital mortality and of preventable cardiac arrest and death on introduction of a pediatric medical emergency team. Pediatr Crit Care Med 2009; 10: 306-12. 5. Gausche M, Lewis RJ. Out-of-hospital endotracheal intubation of children. Jama 2000; 283: 2790-2. 6. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation 2004; 109: 1960-5. 7. Davidovic L, LaCovey D, Pitetti RD. Comparison of 1- versus 2-person bag-valve-mask techniques for manikin ventilation of infants and children. Ann Emerg Med 2005; 46: 37-42. 8. Daugherty RJ, Nadkarni V, Brenn BR. Endotracheal tube size estimation for children with pathological short stature. Pediatr Emerg Care 2006; 22: 710-7. 9. Hofer CK, Ganter M, Tucci M, Klaghofer R, Zollinger A. How reliable is length-based determination of body weight and tracheal tube size in the paediatric age group? The Broselow tape reconsidered. Br J Anaesth 2002; 88: 283-5. 10. Weiss M, Dullenkopf A, Fischer JE, Keller C, Gerber AC. Prospective randomized controlled multi-centre trial of cuffed or uncuffed endotracheal tubes in small children. Br J Anaesth 2009; 103: 867-73. 11. Dullenkopf A, Gerber AC, Weiss M. Fit and seal characteristics of a new paediatric tracheal tube with high 132 volume-low pressure polyurethane cuff. Acta Anaesthesiol Scand 2005; 49: 232-7. 12. Salgo B, Schmitz A, Henze G, et al. Evaluation of a new recommendation for improved cuffed tracheal tube size selection in infants and small children. Acta Anaesthesiol Scand 2006; 50: 557-61. 13. Duracher C, Schmautz E, Martinon C, Faivre J, Carli P, Orliaguet G. Evaluation of cuffed tracheal tube size predicted using the Khine formula in children. Paediatr Anaesth 2008; 18: 113-8. 14. Browning DH, Graves SA. Incidence of aspiration with endotracheal tubes in children. J Pediatr 1983; 102: 582-4. 15. Khine HH, Corddry DH, Kettrick RG, et al. Comparison of cuffed and uncuffed endotracheal tubes in young children during general anesthesia. Anesthesiology 1997; 86: 627-31; discussion 27A. 16. Newth CJ, Rachman B, Patel N, Hammer J. The use of cuffed versus uncuffed endotracheal tubes in pediatric intensive care. J Pediatr 2004; 144: 333-7. 17. Kim JT, Kim HJ, Ahn W, et al. Head rotation, flexion, and extension alter endotracheal tube position in adults and children. Can J Anaesth 2009; 56: 751-6. 18. Cantineau JP, Merckx P, Lambert Y, Sorkine M, Bertrand C, Duvaldestin P. Effect of epinephrine on endtidal carbon dioxide pressure during prehospital cardiopulmonary resuscitation. Am J Emerg Med 1994; 12: 267-70. 19. Ornato JP, Shipley JB, Racht EM, et al. Multicenter study of a portable, hand-size, colorimetric end-tidal carbon dioxide detection device. Ann Emerg Med 1992; 21: 518-23. 20. Somberg JC, Bailin SJ, Haffajee CI, et al. Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia. Am J Cardiol 2002; 90: 853-9. 21. Jones P, Peters MJ, Pinto da Costa N, et al. Atropine for critical care intubation in a cohort of 264 children and reduced mortality unrelated to effects on bradycardia. PLoS One 2013; 8: e57478. 22. Jones P, Dauger S, Denjoy I, et al. The effect of atropine on rhythm and conduction disturbances during 322 133 critical care intubations. Pediatr Crit Care Med 2013; 14: e289-97. 23. Fastle RK, Roback MG. Pediatric rapid sequence intubation: incidence of reflex bradycardia and effects of pretreatment with atropine. Pediatr Emerg Care 2004; 20: 651-5. 24. Zwiener RJ, Ginsburg CM. Organophosphate and carbamate poisoning in infants and children. Pediatrics 1988; 81: 121-6. 25. de Mos N, van Litsenburg RR, McCrindle B, Bohn DJ, Parshuram CS. Pediatric in-intensive-care-unit cardiac arrest: incidence, survival, and predictive factors. Crit Care Med 2006; 34: 1209-15. 26. Srinivasan V, Morris MC, Helfaer MA, Berg RA, Nadkarni VM. Calcium use during in-hospital pediatric cardiopulmonary resuscitation: a report from the National Registry of Cardiopulmonary Resuscitation. Pediatrics 2008; 121: e1144-51. 27. Martin TJ, Kang Y, Robertson KM, Virji MA, Marquez JM. Ionization and hemodynamic effects of calcium chloride and calcium gluconate in the absence of hepatic function. Anesthesiology 1990; 73: 62-5. 28. Broner CW, Stidham GL, Westenkirchner DF, Watson DC. A prospective, randomized, double-blind comparison of calcium chloride and calcium gluconate therapies for hypocalcemia in critically ill children. J Pediatr 1990; 117: 986-9. 29. Niemann JT, Criley JM, Rosborough JP, Niskanen RA, Alferness C. Predictive indices of successful cardiac resuscitation after prolonged arrest and experimental cardiopulmonary resuscitation. Ann Emerg Med 1985; 14: 521-8. 30. Sanders AB, Ewy GA, Taft TV. Prognostic and therapeutic importance of the aortic diastolic pressure in resuscitation from cardiac arrest. Crit Care Med 1984; 12: 871-3. 31. Enright K, Turner C, Roberts P, Cheng N, Browne G. Primary cardiac arrest following sport or exertion in children presenting to an emergency department: chest compressions and early defibrillation can save lives, but is intravenous epinephrine always appropriate? Pediatr Emerg Care 2012; 28: 336-9. 32. Dieckmann RA, Vardis R. High-dose epinephrine in pediatric out-of-hospital cardiopulmonary arrest. 134 Pediatrics 1995; 95: 901-13. 33. Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL. Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial. Resuscitation 2011; 82: 1138-43. 34. Matamoros M, Rodriguez R, Callejas A, et al. In-hospital pediatric cardiac arrest in Honduras. Pediatr Emerg Care 2015; 31: 31-5. 35. Beiser DG, Carr GE, Edelson DP, Peberdy MA, Hoek TL. Derangements in blood glucose following initial resuscitation from in-hospital cardiac arrest: a report from the national registry of cardiopulmonary resuscitation. Resuscitation 2009; 80: 624-30. 36. Valdes SO, Donoghue AJ, Hoyme DB, et al. Outcomes associated with amiodarone and lidocaine in the treatment of in-hospital pediatric cardiac arrest with pulseless ventricular tachycardia or ventricular fibrillation. Resuscitation 2014; 85: 381-6. 37. Dorian P, Cass D, Schwartz B, Cooper R, Gelaznikas R, Barr A. Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation. N Engl J Med 2002; 346: 884-90. 38. Wilson FC, Harpur J, Watson T, Morrow JI. Adult survivors of severe cerebral hypoxia--case series survey and comparative analysis. NeuroRehabilitation 2003; 18: 291-8. 39. Thomson PD, Melmon KL, Richardson JA, et al. Lidocaine pharmacokinetics in advanced heart failure, liver disease, and renal failure in humans. Ann Intern Med 1973; 78: 499-508. 40. Allegra J, Lavery R, Cody R, et al. Magnesium sulfate in the treatment of refractory ventricular fibrillation in the prehospital setting. Resuscitation 2001; 49: 245-9. 41. Hassan TB, Jagger C, Barnett DB. A randomised trial to investigate the efficacy of magnesium sulphate for refractory ventricular fibrillation. Emerg Med J 2002; 19: 57-62. 42. Thel MC, Armstrong AL, McNulty SE, Califf RM, O'Connor CM. Randomised trial of magnesium in inhospital cardiac arrest. Duke Internal Medicine Housestaff. Lancet 1997; 350: 1272-6. 135 43. Vukmir RB, Katz L. Sodium bicarbonate improves outcome in prolonged prehospital cardiac arrest. Am J Emerg Med 2006; 24: 156-61. 44. Lokesh L, Kumar P, Murki S, Narang A. A randomized controlled trial of sodium bicarbonate in neonatal resuscitation-effect on immediate outcome. Resuscitation 2004; 60: 219-23. 45. Duncan JM, Meaney P, Simpson P, Berg RA, Nadkarni V, Schexnayder S. Vasopressin for in-hospital pediatric cardiac arrest: results from the American Heart Association National Registry of Cardiopulmonary Resuscitation. Pediatr Crit Care Med 2009; 10: 191-5. 46. Mann K, Berg RA, Nadkarni V. Beneficial effects of vasopressin in prolonged pediatric cardiac arrest: a case series. Resuscitation 2002; 52: 149-56. 47. Matok I, Vardi A, Augarten A, et al. Beneficial effects of terlipressin in prolonged pediatric cardiopulmonary resuscitation: a case series. Crit Care Med 2007; 35: 1161-4. 48. Perondi MB, Reis AG, Paiva EF, Nadkarni VM, Berg RA. A comparison of high-dose and standard-dose epinephrine in children with cardiac arrest. N Engl J Med 2004; 350: 1722-30. 49. Berg MD, Samson RA, Meyer RJ, Clark LL, Valenzuela TD, Berg RA. Pediatric defibrillation doses often fail to terminate prolonged out-of-hospital ventricular fibrillation in children. Resuscitation 2005; 67: 63-7. 50. Rossano JW, Quan L, Kenney MA, Rea TD, Atkins DL. Energy doses for treatment of out-of-hospital pediatric ventricular fibrillation. Resuscitation 2006; 70: 80-9. 51. Rodriguez-Nunez A, Lopez-Herce J, del Castillo J, Bellon JM. Shockable rhythms and defibrillation during in-hospital pediatric cardiac arrest. Resuscitation 2014; 85: 387-91. 52. Gutgesell HP, Tacker WA, Geddes LA, Davis S, Lie JT, McNamara DG. Energy dose for ventricular defibrillation of children. Pediatrics 1976; 58: 898-901. 53. Meaney PA, Nadkarni VM, Atkins DL, et al. Effect of defibrillation energy dose during in-hospital pediatric cardiac arrest. Pediatrics 2011; 127: e16-23. 136 54. van Haarst AD, van 't Klooster GA, van Gerven JM, et al. The influence of cisapride and clarithromycin on QT intervals in healthy volunteers. Clin Pharmacol Ther 1998; 64: 542-6. 55. Ray WA, Murray KT, Meredith S, Narasimhulu SS, Hall K, Stein CM. Oral erythromycin and the risk of sudden death from cardiac causes. N Engl J Med 2004; 351: 1089-96. 56. Bennett KS, Clark AE, Meert KL, et al. Early oxygenation and ventilation measurements after pediatric cardiac arrest: lack of association with outcome. Crit Care Med 2013; 41: 1534-42. 57. Del Castillo J, Lopez-Herce J, Matamoros M, et al. Hyperoxia, hypocapnia and hypercapnia as outcome factors after cardiac arrest in children. Resuscitation 2012; 83: 1456-61. 58. Ferguson LP, Durward A, Tibby SM. Relationship between arterial partial oxygen pressure after resuscitation from cardiac arrest and mortality in children. Circulation 2012; 126: 335-42. 59. Guerra-Wallace MM, Casey FL, 3rd, Bell MJ, Fink EL, Hickey RW. Hyperoxia and hypoxia in children resuscitated from cardiac arrest. Pediatr Crit Care Med 2013; 14: e143-8. 60. Topjian AA, French B, Sutton RM, et al. Early postresuscitation hypotension is associated with increased mortality following pediatric cardiac arrest. Crit Care Med 2014; 42: 1518-23. 61. Lin YR, Li CJ, Wu TK, et al. Post-resuscitative clinical features in the first hour after achieving sustained ROSC predict the duration of survival in children with non-traumatic out-of-hospital cardiac arrest. Resuscitation 2010; 81: 410-7. 62. Lin YR, Wu HP, Chen WL, et al. Predictors of survival and neurologic outcomes in children with traumatic out-of-hospital cardiac arrest during the early postresuscitative period. J Trauma Acute Care Surg 2013; 75: 439-47. 63. Young MN, Hollenbeck RD, Pollock JS, et al. Higher achieved mean arterial pressure during therapeutic hypothermia is not associated with neurologically intact survival following cardiac arrest. Resuscitation 2015; 88: 158-64. 64. Zaritsky A, Chernow B. Use of catecholamines in pediatrics. J Pediatr 1984; 105: 341-50. 137 65. Bellomo R, Chapman M, Finfer S, Hickling K, Myburgh J. Low-dose dopamine in patients with early renal dysfunction: a placebo-controlled randomised trial. Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Lancet 2000; 356: 2139-43. 66. Ushay HM, Notterman DA. Pharmacology of pediatric resuscitation. Pediatr Clin North Am 1997; 44: 207- 33. 67. Ruffolo RR, Jr., Spradlin TA, Pollock GD, Waddell JE, Murphy PJ. Alpha and beta adrenergic effects of the stereoisomers of dobutamine. J Pharmacol Exp Ther 1981; 219: 447-52. 68. Barton P, Garcia J, Kouatli A, et al. Hemodynamic effects of i.v. milrinone lactate in pediatric patients with septic shock. A prospective, double-blinded, randomized, placebo-controlled, interventional study. Chest 1996; 109: 1302-12. 69. Doherty DR, Parshuram CS, Gaboury I, et al. Hypothermia therapy after pediatric cardiac arrest. Circulation 2009; 119: 1492-500. 70. Fink EL, Clark RS, Kochanek PM, Bell MJ, Watson RS. A tertiary care center's experience with therapeutic hypothermia after pediatric cardiac arrest. Pediatr Crit Care Med 2010; 11: 66-74. 71. Laptook A, Tyson J, Shankaran S, et al. Elevated temperature after hypoxic-ischemic encephalopathy: risk factor for adverse outcomes. Pediatrics 2008; 122: 491-9. 72. Lin JJ, Hsia SH, Wang HS, Chiang MC, Lin KL. Therapeutic hypothermia associated with increased survival after resuscitation in children. Pediatr Neurol 2013; 48: 285-90. 73. Moler FW, Silverstein FS, Holubkov R, et al. Therapeutic hypothermia after out-of-hospital cardiac arrest in children. N Engl J Med 2015; 372: 1898-908. 74. Scholefield BR, Morris KP, Duncan HP, et al. Evolution, safety and efficacy of targeted temperature management after pediatric cardiac arrest. Resuscitation 2015; 92: 19-25. 75. Kessler SK, Topjian AA, Gutierrez-Colina AM, et al. Short-term outcome prediction by electroencephalographic features in children treated with therapeutic hypothermia after cardiac arrest. Neurocrit 138 Care 2011; 14: 37-43. 76. Abend NS, Topjian AA, Kessler SK, et al. Outcome prediction by motor and pupillary responses in children treated with therapeutic hypothermia after cardiac arrest. Pediatr Crit Care Med 2012; 13: 32-8. 77. Fink EL, Berger RP, Clark RS, et al. Serum biomarkers of brain injury to classify outcome after pediatric cardiac arrest. Crit Care Med 2014; 42: 664-74. 78. Moler FW, Donaldson AE, Meert K, et al. Multicenter cohort study of out-of-hospital pediatric cardiac arrest. Crit Care Med 2011; 39: 141-9. 79. Nishisaki A, Sullivan J, 3rd, Steger B, et al. Retrospective analysis of the prognostic value of electroencephalography patterns obtained in pediatric in-hospital cardiac arrest survivors during three years. Pediatr Crit Care Med 2007; 8: 10-7. 80. Pfeifer R, Borner A, Krack A, Sigusch HH, Surber R, Figulla HR. Outcome after cardiac arrest: predictive values and limitations of the neuroproteins neuron-specific enolase and protein S-100 and the Glasgow Coma Scale. Resuscitation 2005; 65: 49-55. 81. Topjian AA, Lin R, Morris MC, et al. Neuron-specific enolase and S-100B are associated with neurologic outcome after pediatric cardiac arrest. Pediatr Crit Care Med 2009; 10: 479-90. 139 Part 7. Neonatal Resuscitation The following is a summary of the 2015 Korean Neonatal Resuscitation guidelines. An extensive review of scientific evidence by experts of Neonatal Resuscitation Committee for the 2015 Korean Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care including neonatologists, nurse, obstetrician, perinatologist, and anesthesiologist was performed to update the 2011 Korean Neonatal Resuscitation guidelines. Overview It has been reported that approximately 85% of term babies will start spontaneous breathing within 10-30 seconds after birth, an additional 10% will respond to drying and stimulation for breathing, about 3% will breathe after positive-pressure ventilation (PPV), 2% will need intubation, and 0.1% will require chest compression and/or epinephrine during transition to extra-uterine life. 1-3 One of the key factors for neonatal resuscitation is anticipation. Determining who will require resuscitation, what equipment needs to be prepared, whom to join, and how each member should participate in the resuscitation are all important factors in anticipating neonatal resuscitation. Beginning resuscitation with antenatal counseling and a team briefing are also important.4-5 The vital signs used to identify the need for neonatal resuscitation and to assess response to resuscitation are heart rate and respiration. Heart rate could be checked by either auscultating along the left side of chest or palpating the umbilical cord base. If the heart rate cannot be determined by auscultation/palpation and the baby is not vigorous, pulse oximetry (could underestimate heart rate) or cardiac monitoring can be used for a better estimation of heart rate. 6-9 Oxygen saturation determined by pulse oximetry indicates color, a third vital sign. The most sensitive indicator of a successful resuscitation is an increase in heart rate. The critical factor to achieve successful neonatal resuscitation is an effective ventilation. 140 Figure 7-1. Neonatal Resuscitation Algorithm HR, heart rate; PPV, positive pressure ventilation; SpO2, oxygen saturation; ECG, electrocardiography; CPAP, continuous positive airway pressure 141 Newly born term infants who are breathing or crying and have a good tone immediately after birth should be dried and taken to the mother for routine care, with continuous evaluation. However, preterm or term infants who are not breathing or crying and have poor tone should be dried, stimulated to initiate breathing, and kept in a position that best opens the airway. It is recommended that the temperature of newly born non-asphyxiated infants should be maintained between 36.5°C and 37.5°C after birth through resuscitation or stabilization, and admission temperature of non-asphyxiated infants should be recorded, as it is a strong predictor of mortality and morbidity for all gestations.9 Hypothermic infants with a temperature less than 36°C on hospital admission could be rewarmed using either the rapid (0.5°C/hour or greater) or the slow (less than 0.5°C/hour) rewarming method. After the aforementioned ”initial care,” the resuscitator should determine the heart rate and if the newborn infant’s heart rate is lower than 100 beats/minute or if the infant is gasping or is apneic, providing an effective ventilation with a face mask or endotracheal intubation (recommending intubation prior to beginning chest compression) is essential. If the newly born infant has a heart rate higher than 100 beats/minute and shows labored breathing or persistent cyanosis, consider using continuous positive airway pressure (CPAP).10-12 Only approximately 60 seconds after birth is allotted to initiate ventilation after determination of heart rate. When PPV begins, consider using ECG monitoring for accurate assessment of the heart rate. After 30 seconds of PPV that initiates chest movement, the heart rate is reassessed. If the heart rate is lower than 60 beats/minute, corrective steps should be taken to ensure adequate ventilation(Figure 7-1).13 Alternative airways such as endotracheal intubation (if face mask was used) or laryngeal mask (if intubation is unsuccessful or not possible for late preterm infants of more than 34 weeks gestation or in case of term infants) can be inserted.14 If no improvement in heart rate is seen, begin 100% oxygen and chest compressions. Chest compressions at lower 1/3 of the sternum using 3:1 compression-to-ventilation ratio remains unchanged. Superimposed thumbs may be a better technique for cardiac compression in newborns and can be continued from the head of the bed while accessing the umbilical line. Reassessment of heart rate is performed after 60 seconds of chest compression, at which time medications should be administered. Medication is rarely indicated during neonatal resuscitation because bradycardia during newborn resuscitation is usually due to inadequate lung inflation or hypoxemia, and initiating ventilation is the most critical and important step to resolution. Epinephrine remains a major medication. The recommended fluid for acute hypovolemia is normal saline or type-0-negative blood via an 142 umbilical venous catheter or via an intraosseous needle, if required, in term and preterm newborns. A newly born infant with meconium-stained amniotic fluid does not need a routine intubation for tracheal suctioning even when non-vigorous. Instead, adequate oxygenation and ventilation should be considered first.15- 19 A few changes have been made with regard to resuscitation of preterm infants. With regard to cord clamping, delaying umbilical cord clamping for more than 30 seconds is suggested for preterm infants not requiring resuscitation. For preterm infants requiring resuscitation, there is insufficient evidence supporting a delayed cord clamping at birth. Routine use of umbilical cord milking for infants of gestational age 28 weeks or less is not recommended; however, it may be considered on individual basis or in research settings.4,9,20 Increasing the room temperature to approximately 23-25°C in preparation for the birth of preterm infants and using radiant warmer, plastic wrap, warm blankets, hat, thermal mattress, warm humidified gases are recommended for preterm infants of less than 32 weeks of gestation to reduce hypothermia. 21,22 It is recommended that hyperthermia (38°C) should be avoided. Regarding the use of oxygen, resuscitation of newborns of 35-week gestation or greater should begin with 21% oxygen. Resuscitation of newborns of less than 35 weeks of gestation should begin with 21-30% oxygen.23-25 Free-flow oxygen administration may be initiated using an oxygen blender at 30%, and titrate oxygen to achieve preductal oxygen saturation targets for healthy term infants after vaginal delivery.26 When PPV is required for resuscitating preterm infants, it is preferable to use positive end expiratory pressure (PEEP) devices to inflate lungs at 5 cm H2O between the positive pressures.27 The routine use of initial sustained inflation longer than 5 seconds for preterm infants without spontaneous respiration is not recommended.9 Post–cardiac arrest care Once newborns who required resuscitation are stabilized, they should be hospitalized where close monitoring is possible. Infants of more than 36 weeks of gestation with evolving moderate-to-severe hypoxic ischemic encephalopathy should be considered for therapeutic hypothermia at an institution where multidisciplinary care and well-defined protocols can be applied (i.e., cooling within 6 hours, temperature control at 33°C-34°C for 72 143 hours, and rewarming over, at least, 4 hours). 5 Discontinuing resuscitation Evidence for delivery prognostic score for preterm infants of less than 25 weeks of gestation is insufficient to support its use. It may be reasonable to stop resuscitation for newborns with an Apgar score of 0 after 10 minutes of optimal resuscitation; however, the decision to stop resuscitation should be individualized.28 If spontaneous respiration is not seen or Apgar scores of 1 to 3 at 20 minutes of age in newborns with greater than 34 weeks of gestation, it may be reasonable to stop resuscitation in settings with limited resources.9 In all cases, risk and benefits of attempting resuscitation and life-sustaining treatment should be discussed with parents, and decision should be made in the best interest of the infant. Educational program Further refinement in the current instructor program is needed to prepare instructors to train providers. It is suggested that neonatal resuscitation training for neonatal resuscitation providers be conducted as frequently as 6 months or more29-30, however, the best interval for renewal is to be determined. 144 References 1. Ersdal HL, Mduma E, Svensen E, Perlman JM. Early initiation of basic resuscitation interventions including face mask ventilation may reduce birth asphyxia related mortality in low-income countries: a prospective descriptive observational study. Resuscitation 2012;83:869–73. 2. Perlman JM, Risser R. Cardiopulmonary resuscitation in the delivery room. Associated clinical events. Arch Pediatr Adolesc Med 1995;149:20–25. 3. Barber CA, Wyckoff MH. Use and efficacy of endotracheal versus intravenous epinephrine during neonatal cardiopulmonary resuscitation in the delivery room. Pediatrics 2006;118:1028–34. 4. Perlman JM, Wyllie J, Kattwinkel J, et al. Part 11: neonatal resuscitation: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation 2010;122(suppl 2):S516–38. 5. Wyllie J, Perlman JM, Kattwinkel J, et al. Part 11: neonatal resuscitation: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Resuscitation 2010;81 suppl 1:e260–8. 6. Dawson JA, Saraswat A, Simionato L, et al. Comparison of heart rate and oxygen saturation measurements from Masimo and Nellcor pulse oximeters in newly born term infants. Acta Paediatr 2013;102:955–60. 7. Kamlin CO, Dawson JA, O’Donnell CP, et al. Accuracy of pulse oximetry measurement of heart rate of newborn infants in the delivery room. J Pediatr 2008;152:756–60. 8. van Vonderen JJ, Hooper SB, Kroese JK, et al. Pulse oximetry measures a lower heart rate at birth compared with electrocardiography. J Pediatr 2015;166:49–53. 9. Perlman JM, Wyllie J, Kattwinkel J, et al. Part 7: neonatal resuscitation: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation 2015;132(suppl 1):S204–41. 10. Morley CJ, Davis PG, Doyle LW, et al. Nasal CPAP or intubation at birth for very preterm infants. N Engl J Med 2008;358:700–8. 11. SUPPORT Study Group of the Eunice Kennedy Shriver NICHD Neonatal Research Network, Finer NN, Carlo WA, Walsh MC, et al. Early CPAP versus surfactant in extremely preterm infants. N Engl J Med 145 2010;362:1970–79. 12. Dunn MS, Kaempf J, de Klerk A, et al. Randomized trial comparing 3 approaches to the initial respiratory management of preterm neonates. Pediatrics 2011;128:e1069– 76. 13. Kattwinkel J, Perlman JM, Aziz K, et al. Part 15: neonatal resuscitation: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122(suppl 3):S909–S19. 14. Esmail N, Saleh M. Laryngeal mask airway versus endotracheal intubation for Apgar score improvement in neonatal resuscitation. Egypt J Anesth 2002;18:115–21. 15. Chettri S, Adhisivam B, Bhat BV. Endotracheal suction for nonvigorous neonates born through meconium stained amniotic fluid: a randomized controlled trial. J Pediatr 2015;166:1208–13. 16. Davis RO, Philips JB 3rd, Harris BA Jr, Wilson ER, Huddleston JF. Fatal meconium aspiration syndrome occurring despite airway management considered appropriate. Am J Obstet Gynecol 1985;151:731–36. 17. Dooley SL, Pesavento DJ, Depp R, Socol ML, Tamura RK, Wiringa KS. Meconium below the vocal cords at delivery: correlation with intrapartum events. Am J Obstet Gynecol 1985;153:767–70. 18. Rossi EM, Philipson EH, Williams TG, Kalhan SC. Meconium aspiration syndrome: intrapartum and neonatal attributes. Am J Obstet Gynecol 1989;161:1106–10. 19. Yoder BA. Meconium-stained amniotic fluid and respiratory complications: impact of selective tracheal suction. Obstet Gynecol 1994;83:77–84. 20. Wyllie J, Perlman JM, Kattwinkel J,. Part 7: neonatal resuscitation: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Resuscitation 2015;95:e169-201. 21. Chawla S, Amaram A, Gopal SP, Natarajan G. Safety and efficacy of Trans-warmer mattress for preterm neonates: results of a randomized controlled trial. J Perinatol 2011;31:780–4. 22. te Pas AB, Lopriore E, Dito I, Morley CJ, Walther FJ. Humidified and heated air during stabilization at birth improves temperature in preterm infants. Pediatrics 2010;125:e1427–32. 23. Armanian AM, Badiee Z. Resuscitation of preterm newborns with low concentration oxygen versus high concentration oxygen. J Res Pharm Pract 2012;1:25–9. 24. Kapadia VS, Chalak LF, Sparks JE, Allen JR, Savani RC, Wyckoff MH. Resuscitation of preterm neonates 146 with limited versus high oxygen strategy. Pediatrics 2013;132: e1488–96. 25. Rook D, Schierbeek H, Vento M, et al. Resuscitation of preterm infants with different inspired oxygen fractions. J Pediatr 2014;164:1322–6. 26. Mariani G, Dik PB, Ezquer A, et al. Pre-ductal and post-ductal O2 saturation in healthy term neonates after birth. J Pediatr 2007;150:418–21. 27. Szyld E, Aguilar A, Musante GA, et al. Comparison of devices for newborn ventilation in the delivery room. J Pediatr 2014;165: 234–39. 28. Harrington DJ, Redman CW, Moulden M, Greenwood CE. The long-term outcome in surviving infants with Apgar zero at 10 minutes: a systematic review of the literature and hospital-based cohort. Am J Obstet Gynecol 2007;196:463. 29. Ernst KD, Cline WL, Dannaway DC, Davis EM, Anderson MP, Atchley CB, Thompson BM. Weekly and consecutive day neonatal intubation training: comparable on a pediatrics clerkship. Acad Med 2014;89:505–510. 30. Mosley CM, Shaw BN. A longitudinal cohort study to investigate the retention of knowledge and skills following attendance on the Newborn Life support course. Arch Dis Child 2013;98:582–6. 147 Part 8. Guideline for Cardiopulmonary Resuscitation Education Cardiac arrest is a major social and public healthcare issue. According to the 2015 statistics of the Centers for Disease Control and Prevention, 45.1 persons per 100,000 population had a cardiac arrest and the rate of resuscitation for cardiac arrest is 4.8%, which is low in comparison with the economic scale of the country.1 Moreover, the mean prevalence of patients discharged with cerebral performance categories (CPC) 1 or 2, which indicate good neurological prognosis for patients who had cardiac arrest, was only 2.3%.2 This is also lower than the 9.6% of the overall survival rate to hospital discharge reported in a Cardiac Arrest Registry to Enhance Survival (CARES) research that covered the entire United States of America from 2005 to 2010 and the 8.9% reported for Osaka, Japan, from 2007 to 2009.3, 4 In addition, resuscitation rates differ by five- to six-fold at the maximum between regions, thus requiring multilateral considerations. In order to successfully apply the newly introduced 2015 Cardiopulmonary Resuscitation (CPR) Guidelines to the society, a well-planned integrated application strategy is required, along with an educational strategy as a core factor. Key Recommendation in CPR Education 1. Setting the goal of education The objective of CPR education should be focused on ensuring that students obtain knowledge and skill in CPR, which can be immediately applied to actual cardiac arrest patients, and to maintain these knowledge and skill for a considerable amount of time. Every educational step should be geared toward helping students effectively achieve this objective. 2. Practice while watching method In order to minimize the side effects due to alterations of the obtained education according to the performance 148 and skill level of different CPR instructors, video or computer-based (self) learning programs are recommended as media thereby students can obtain knowledge and skill in CPR, with little or no intervention at all by the instructor..5, 6 Especially in terms of learning the basic CPR, including directions for automated external defibrillator, practicing while watching is essential. 3. Skill-learning centralized education Delivering the knowledge is necessary. However, most of the time, sessions should be allocated and conducted to help students to enable them to repeatedly practice and eventually acquire CPR skills. The objective is to enable the students to learn to effectively perform CPR within a given time during the education without additional out-of-class practice. Unnecessary lectures should be minimized. 4. Re-education cycle Both the general public and medical personnel who do not often perform CPR easily forget their knowledge and skill in CPR after 3 to 6 months from completing the basic and expert resuscitation courses.5, 6 In order to maintain their knowledge and performance of the CPR, targets in need of assistance are identified during the education to be introduced with re-educations or re-evaluations via convenient means such as online selflearning program or video sessions, at the longest term of 6-month cycle. Accumulating evidence shows that the existing 2-year cycle for license renewal in basic and expert resuscitation is not adequate. However, this reeducation cycle is yet to be optimized because of insufficient basis. 5. Use of a measurable skill evaluation tool It is recommended that the degrees of depth, frequency, and full relaxation in chest compressions during practice and evaluation in CPR education should be numerically measured in order to monitor the skill CPR level while providing feedbacks by utilizing a prompt or a measuring device. In case a device for feedback is not 149 available, auditory guidance (metronome or music) can be used.7, 8 6. Reinforced education for non-technical skills Considering actual CPR situations, wherein more than two rescuers rather than a single rescuer perform the resuscitation in absolute majority, non-technical skills greatly affect the result of the CPR, such as teamwork between the members of the CPR team, leadership for tuning up the activities within the team, and patient turnover between team members, must be included in the education.9, 10 7. Debriefing and seminar-type delivery Debriefings, inquiries, and discussions at the end of each step or the entire CPR education are strongly recommended, as summary of the education can greatly improve the CPR performance of an individual or team.11 Devising an effective educational method 1. Using realistic dummy As CPR cannot be applied to a real person during skill practice, dummies are used. The currently used dummies are very similar in function to real patients owing to the rapid advancement in scientific technology. A basic dummy is enough for the purpose of delivering and practicing the basic knowledge and skill in CPR. However, when education is aimed at training for expert-level CPR through diversified scenarios, more-realistic dummies are recommended.12 As a result, the purpose, target, costs, and benefits of education should be equally considered to determine the type of dummy to use. 150 2. Checklists/means to assist memorization The use of checklists/means to assist memorization among students shows a positive effect on upskilling their CPR performance. To further utilize this strong point, both the student and the instructor must be well acquainted with using the checklists/means to assist memorization. 3. Feedback device It is recommended that a device be used for giving direct feedbacks on speed, depth, relaxation, hand position during chest compression in CPR education.13, 14 If such a feedback device is not available, a feedback device based on auditory guidance such as music or metronome is recommended in order to improve the speed of chest compression.15 4. Debriefing Debriefing refers to a time of structuring the educational experience through discussions, debates, and feedbacks at the end of the simulation process. Many studies show that debriefing is the most important step in simulationtype educations.16 Considering this, debriefing must be essentially included in CPR education and recommended after the students undergo actual cases of CPR. 5. Roles of social media technology Various social media technologies have been widely used recently. Interest is increasing on a method in which people who are able and willing to conduct CPR would be notified of a nearby OHCA patient by actively utilizing social media.17, 18 It is suggested that for this method, scientific technology and social media should be used to notify people who are able and willing to conduct CPR when they are near a suspected OHCA patient. 151 Reference 1. Available at: http://www.cdc.go.kr/. Accessed October 14, 2015. 2. Ahn KO, Shin SD, Suh GJ, et al. Epidemiology and outcomes from non-traumatic out-of-hospital ca rdiac arrest in Korea: A nationwide observational study. Resuscitation 2010; 81: 974-81. 3. McNally B, Robb R, Mehta M, et al. Out-of-hospital cardiac arrest surveillance --- Cardiac Arrest R egistry to Enhance Survival (CARES), United States, October 1, 2005--December 31, 2010. MMWR Su rveill Summ 2011; 60: 1-19. 4. Shin SD, Kitamura T, Hwang SS, et al. Association between resuscitation time interval at the scene and neurological outcome after out-of-hospital cardiac arrest in two Asian cities. Resuscitation 2014; 8 5: 203-10. 5. Lynch B, Einspruch EL, Nichol G, Becker LB, Aufderheide TP, Idris A. Effectiveness of a 30-min CPR self-instruction program for lay responders: a controlled randomized study. Resuscitation 2005; 67: 31-43. 6. Einspruch EL, Lynch B, Aufderheide TP, Nichol G, Becker L. Retention of CPR skills learned in a traditional AHA Heartsaver course versus 30-min video self-training: a controlled randomized study. R esuscitation 2007; 74: 476-86. 7. Rawlins L, Woollard M, Williams J, Hallam P. Effect of listening to Nellie the Elephant during CP R training on performance of chest compressions by lay people: randomised crossover trial. BMJ 2009; 339: b4707. 8. Woollard M, Poposki J, McWhinnie B, Rawlins L, Munro G, O'Meara P. Achy breaky makey wake y heart? A randomised crossover trial of musical prompts. Emerg Med J 2012; 29: 290-4. 9. Bhanji F, Mancini ME, Sinz E, et al. Part 16: education, implementation, and teams: 2010 America n Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 122: S920-33. 152 10. Soar J, Mancini ME, Bhanji F, et al. Part 12: Education, implementation, and teams: 2010 Internat ional Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Tr eatment Recommendations. Resuscitation 2010; 81 Suppl 1: e288-330. 11. Edelson DP, Litzinger B, Arora V, et al. Improving in-hospital cardiac arrest process and outcomes with performance debriefing. Arch Intern Med 2008; 168: 1063-9. 12. Lo BM, Devine AS, Evans DP, et al. Comparison of traditional versus high-fidelity simulation in t he retention of ACLS knowledge. Resuscitation 2011; 82: 1440-3. 13. Yeung J, Davies R, Gao F, Perkins GD. A randomised control trial of prompt and feedback device s and their impact on quality of chest compressions--a simulation study. Resuscitation 2014; 85: 553-9. 14. Cheng A, Brown LL, Duff JP, et al. Improving cardiopulmonary resuscitation with a CPR feedbac k device and refresher simulations (CPR CARES Study): a randomized clinical trial. JAMA Pediatr 20 15; 169: 137-44. 15. Kim SC, Hwang SO, Cha KC, et al. A simple audio-visual prompt device can improve CPR perfo rmance. J Emerg Med 2013; 44: 128-34. 16. Cheng A, Hunt EA, Donoghue A, et al. Examining pediatric resuscitation education using simulatio n and scripted debriefing: a multicenter randomized trial. JAMA Pediatr 2013; 167: 528-36. 17. Zijlstra JA, Stieglis R, Riedijk F, Smeekes M, van der Worp WE, Koster RW. Local lay rescuers with AEDs, alerted by text messages, contribute to early defibrillation in a Dutch out-of-hospital cardia c arrest dispatch system. Resuscitation 2014; 85: 1444-9. 18. Ringh M, Rosenqvist M, Hollenberg J, et al. Mobile-phone dispatch of laypersons for CPR in outof- hospital cardiac arrest. N Engl J Med 2015; 372: 2316-25.