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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 ¡Ã5 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 ¡Ã100 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¡ÆC,
whereas the 2015 guidelines were updated to recommend a target of 32–36¡ÆC for ¡Ã24 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
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3. Aneman A, Frost SA, Parr MJ, Hillman KM. Characteristics and outcomes of patients admitted to ICU
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4. Hansen CM, Kragholm K, Granger CB, et al. The role of bystanders, first responders, and emergency medical
service providers in timely defibrillation and related outcomes after out-of-hospital cardiac arrest: Results from
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5. Holmberg M, Holmberg S, Herlitz J. Incidence, duration and survival of ventricular fibrillation in out-ofhospital
cardiac arrest patients in sweden. Resuscitation 2000; 44: 7-17.
6. Strohle M, Paal P, Strapazzon G, Avancini G, Procter E, Brugger H. Defibrillation in rural areas. Am J Emerg
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7. Nielsen N, Wise MP, Cronberg T. Targeted Temperature Management for Cardiac Arrest--Reply. JAMA
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8. Rab T, Kern KB, Tamis-Holland JE, et al. Cardiac Arrest: A Treatment Algorithm for Emergent Invasive
Cardiac Procedures in the Resuscitated Comatose Patient. J Am Coll Cardiol 2015; 66: 62-73.
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Med Clin North Am 2015; 33: 691-712.
10. Roberts BW, Kilgannon JH, Mitchell JA, et al. Emergency department inter-hospital transfer for postcardiac
arrest care: initial experience with implementation of a regional cardiac resuscitation center in the
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11. Berg RA, Hemphill R, Abella BS, et al. Part 5: adult basic life support: 2010 American Heart Association
Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010; 122:
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cardiopulmonary resuscitation: a prospective, randomized simulator-based trial. Swiss Med Wkly 2013; 143:
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during cardiopulmonary resuscitation: improved outcome during a simulated single lay-rescuer scenario.
Circulation 2002; 105: 645-9.
14. Vadeboncoeur T, Stolz U, Panchal A, et al. Chest compression depth and survival in out-of-hospital cardiac
arrest. Resuscitation 2014; 85: 182-8.
15. 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.
16. Beesems SG, Wijmans L, Tijssen JG, Koster RW. Duration of ventilations during cardiopulmonary
resuscitation by lay rescuers and first responders: relationship between delivering chest compressions and
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external defibrillator cardiopulmonary resuscitation protocol on outcome from out-of-hospital cardiac arrest.
Circulation 2010; 121: 1614-22.
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out-of-hospital shockable cardiac arrest. Circulation 2011; 124: 58-66.
19. Perkins GD, Walker G, Christensen K, Hulme J, Monsieurs KG. Teaching recognition of agonal breathing
improves accuracy of diagnosing cardiac arrest. Resuscitation 2006; 70: 432-7.
20. Tanaka Y, Taniguchi J, Wato Y, Yoshida Y, Inaba H. The continuous quality improvement project for
38
telephone-assisted instruction of cardiopulmonary resuscitation increased the incidence of bystander CPR and
improved the outcomes of out-of-hospital cardiac arrests. Resuscitation 2012; 83: 1235-41.
21. Sayre MR, Berg RA, Cave DM, et al. Hands-only (compression-only) cardiopulmonary resuscitation: a call
to action for bystander response to adults who experience out-of-hospital sudden cardiac arrest: a science
advisory for the public from the American Heart Association Emergency Cardiovascular Care Committee.
Circulation 2008; 117: 2162-7.
22. Group S-Ks. Cardiopulmonary resuscitation by bystanders with chest compression only (SOS-KANTO): an
observational study. Lancet 2007; 369: 920-6.
23. Abe T, Tokuda Y, Ishimatsu S, group S-Ks. Predictors for good cerebral performance among adult survivors
of out-of-hospital cardiac arrest. Resuscitation 2009; 80: 431-6.
24. Iwami T, Kawamura T, Hiraide A, et al. Effectiveness of bystander-initiated cardiac-only resuscitation for
patients with out-of-hospital cardiac arrest. Circulation 2007; 116: 2900-7.
25. Stiell IG, Brown SP, Christenson J, et al. What is the role of chest compression depth during out-of-hospital
cardiac arrest resuscitation? Crit Care Med 2012; 40: 1192-8.
26. 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 ¥á- and ¥â-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. 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.
6. Chen YS, Lin JW, Yu HY, et al. Cardiopulmonary resuscitation with assisted extracorporeal life-su
pport versus conventional cardiopulmonary resuscitation in adults with in-hospital cardiac arrest: an obs
ervational study and propensity analysis. Lancet 2008;372:554-61.
7. Sakamoto T, Morimura N, Nagao K, et al. Extracorporeal cardiopulmonary resuscitation versus con
ventional cardiopulmonary resuscitation in adults with out-of-hospital cardiac arrest: a prospective obser
vational study. Resuscitation 2014;85:762-8.
8. 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.
9. 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.
10. Strote JA, Maynard C, Olsufka M, et al. Comparison of role of early (less than six hours) to late
r (more than six hours) or no cardiac catheterization after resuscitation from out-of-hospital cardiac arr
est. Am J Cardiol 2012;109:451-4.
11. Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33 degrees C ve
56
rsus 36 degrees C after cardiac arrest. N Engl J Med 2013;369:2197-206.
12. Hollenbeck RD, McPherson JA, Mooney MR, et al. Early cardiac catheterization is associated wit
h improved survival in comatose survivors of cardiac arrest without STEMI. Resuscitation 2014;85:88-
95.
13. Grasner JT, Meybohm P, Lefering R, et al. ROSC after cardiac arrest--the RACA score to predict
outcome after out-of-hospital cardiac arrest. Eur J Heart 2011;32:1649-56.
14. Bro-Jeppesen J, Kjaergaard J, Wanscher M, et al. 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.
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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 ¡Ã 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 ¡Ã90 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¡ÆC
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¡ÆC) 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¡ÆC) has been suggested as another target
temperature since a large, well-conducted RCT compared the target temperature levels of 33¡ÆC and 36¡ÆC, as it
found that the neurological outcome and survival at 6 months after ROSC were not improved when the
temperature was controlled at 36¡ÆC versus 33¡ÆC.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¡ÆC and 36¡ÆC 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¡ÆC) or ultra-mild hypothermia
(36¡ÆC) 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¡ÆC per hour, which has been used often in previous studies41,42,48,
and maintain normothermia (36.5~37.5¡ÆC) 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
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100. Lee BK, Jeung KW, Lee HY, Jung YH, Lee DH. Combining brain computed tomography and serum neuron
85
specific enolase improves the prognostic performance compared to either alone in comatose cardiac arrest
survivors treated with therapeutic hypothermia. Resuscitation 2013;84:1387-92.
101. Kim SH, Choi SP, Park KN, Youn CS, Oh SH, Choi SM. Early brain computed tomography findings are
associated with outcome in patients treated with therapeutic hypothermia after out-of-hospital cardiac arrest.
Scand J Trauma Resusc Emerg Med 2013;21:57.
102. Els T, Kassubek J, Kubalek R, Klisch J. Diffusion-weighted MRI during early global cerebral hypoxia: a
predictor for clinical outcome? Acta Neurol Scand 2004;110:361-7.
103. Mlynash M, Campbell DM, Leproust EM, et al. Temporal and spatial profile of brain diffusion-weighted
MRI after cardiac arrest. Stroke 2010;41:1665-72
104. Jorgensen EO, Holm S. The natural course of neurological recovery following cardiopulmonary
resuscitation. Resuscitation 1998;36:111-22.
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Part 5. 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
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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.
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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
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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,
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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
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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.
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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
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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.
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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).
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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
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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
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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
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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.
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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
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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
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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
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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.
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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
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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
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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
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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
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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
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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.
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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
¥ìg/kg/min) prominently resulting in beta adrenergic activity and higher doses (>0.3 ¥ìg/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
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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
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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
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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 ¡Ã100–
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
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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 ¡Ã3 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 ¡Ã1
year old or weigh >10 kg, and the pediatric size is used for infants who are <1 year old or weigh <10 kg.
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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
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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 ¡Ã100–
120 per minute, and the second rescuer should perform breathing every 6 seconds (10 per minute). If there are
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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
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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 ¥ìg/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 ¥ìg/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 ¥ìg/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 ¥ìg/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 ¥ìg/kg/min, dopamine induces excessive vasoconstriction and renovascular dilatation disappears.
Therefore, epinephrine or dobutamine are recommended in cases where >20 ¥ìg/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 ¥ìg/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¡ÆC, or to increase above 37.5¡ÆC, 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¡ÆC 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
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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¡ÆC and 37.5¡ÆC 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¡ÆC on hospital admission
could be rewarmed using either the rapid (0.5¡ÆC/hour or greater) or the slow (less than 0.5¡ÆC/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¡ÆC 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¡ÆC) 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¡ÆC-34¡ÆC 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
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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;
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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.

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