COMENIUS UNIVERSITY IN BRATISLAVA
FACULTY OF MEDICINE
PROGRESS IN POST-RESUSCITATION CARE ACCORDING ERC GUIDELINES 2015
2018Michaela – Chrysanthi Vittoraki
COMENIUS UNIVERSITY IN BRATISLAVA
FACULTY OF MEDICINE
UNIVERZITA KOMENSKÉHO V BRATISLAVE
Progress in Post-Resuscitation Care According ERC Guidelines 2015 /
Pokroky v post-resuscita?nej starostlivosti podl’a odporú?aní ERC 2015
Diploma Thesis / Diplomová Práca
Study programme:General medicine / Lekárska fakulta
Study branch:7.1.1.General Medicine
Department:2nd Department of Anesthesiology and Intensive Medicine / II. klinika anesteziológie a intenzívnej medicíny LF UK a OÚSA
Supervisor / Školite?:doc. MUDr. Roman Záhorec, CSc.
BRATISLAVA, 2018Michaela – Chrysanthi Vittoraki
Vittoraki Michaela-Chrysanthi: Progress in Post-Resuscitation Care according ERC Guidelines 2015 Diploma thesis.
Comenius University in Bratislava. Faculty of medicine; 2nd Department of Anesthesiology and Intensive Medicine.
Supervisor: Doc. MUDr. Roman Záhorec, CSc.
Bratislava: 2018, xxx pages
The main aim of this thesis is to describe the changes in Post-Resuscitation Care between the European Resuscitation Council’s Guidelines for Resuscitation of 2010 and 2015. It provides a thorough overview of the changes and aims to emphasize the development of the ERC Guidelines throughout the years. The importance of this thesis lies upon the crucial role of Post-Resuscitation Care in the amelioration of the prognosis and quality of life of the patient after an acute incident. This thesis sets as a goal to bring to the fore the Post-Resuscitation Care and accentuate its gravity among the European Resuscitation Council’s Guidelines.
Key words: European Resuscitation Council, guidelines, post-resuscitation care, post-resuscitation disease
Vittoraki Michaela-Chrysanthi: Pokrok v postresuscita?nej starostlivosti pod?a ERC odporú?aní 2015 Diplomová práca.
Univerzita Komenského, Bratislava. Lekárska fakulta; II. klinika anesteziológie a intenzívnej medicíny LF UK a OÚSA.
Školite?: Doc. MUDr. Roman Záhorec, CSc.
Bratislava: 2018, xxx strán
Hlavným cielom tejto práce je popísa? zmeny v postresuscita?nej starostlivosti medzi Odporú?aniami Európskej resuscita?nej rady pre resuscitáciu rokov 2010 a 2015. Poskytuje dôkladný preh?ad zmien a cie?ov na zdôraznenie vývoja ERC odporú?aní v priebehu rokov. Dôležitos? tejto tézy spo?íva v k?ú?ovej úlohe postresuscita?nej starostlivosti v zlepšení prognózy a kvality života pacienta po akútnej udalosti. Táto téza si dáva za úlohu priviez? do popredia postresuscita?nú starostlivos? a zdôrazni? jej váhu medzi Odporú?aniami Európskej resuscita?nej rady.
K?ú?ové slová: Európska resuscita?ná rada, odporú?ania, postresuscitácia
This dissertation is submitted for the degree of Doctor of General Medicine at Comenius University in Bratislava. The diploma thesis was conducted under the supervision of doc. MUDr. Roman Záhorec, CSc. in the second Department of Anesthesiology and Intensive Medicine, in Faculty of Medicine of Comenius University, between November 2016 and October 2018. This work is to the best of my knowledge original, except where acknowledgements and references are made to previous work. Neither this, nor any substantially similar dissertation has been or is being submitted for any other degree, diploma or other qualification at any other university. The theme of Progress in Post-Resuscitation Care according European Resuscitation Council’s Guidelines of 2015 was chosen in order to present and prove the significance of -not only resuscitation- but also post-resuscitation treatment of the patient. The aim is to focus on the steps followed after resuscitation and to make evident their importance for the better prognosis and quick recovery of the patient after acute incidents.
I would like to express my sincere gratitude to my supervisor, Doc. MUDr Roman Záhorec CSc., for his continuous support during the completion of my diploma thesis. His patience, motivation, immense knowledge and guidance helped me engrave the path towards the best understanding of the importance of post-resuscitation care and made me appreciate to the fullest the field of anesthesiology and intensive care medicine.
I would also like to thank my godfather, Dr. Antonios Gypakis MSc., MBA, PhD., for always showing his support and care. His experience on writing scientific papers and his willingness to share his ideas and opinions were invaluable for the completion of my thesis.
Last but not least, I would like to thank my family for always being by my side throughout the six years of my studies, showing their unconditional love and support.
ABBREVIATIONS AND SYMBOLS
Airway, Breathing Circulation, Disability, Exposure
Adult advanced cardiovascular life support
Acute coronary syndrome
Automated external defibrillation
American heart association
Advanced life support
Acute myocardial infarction
Australian and New Zealand committee on resuscitation
Acute respiratory distress syndrome
Basic life support
Cerebral metabolic rate of oxygen
Central nervous system
Cardiac output/cardiac index
Chronic obstructive pulmonary disease
Consensus on science and treatment recommendations
Cerebral perfusion pressure
Continuous quality improvement
Computed tomography pulmonary angiogram
Systemic oxygen delivery
Mean arterial pressure
Montreal Cognitive Assessment
Multiple organ dysfunction syndrome
National resuscitation council
Non ST-elevation myocardial infarction
Out-of-hospital cardiac arrest
Pediatric basic life support
Post-cardiac arrest syndrome
Percutaneous coronary intervention
Pulseless electrical activity
Resuscitation council of Asia
Resuscitation council of Southern Africa
Randomized controlled trials
Return of spontaneous circulation
WLST: Diffusion weighted imaging
Emergency cardiovascular care
Extracorporeal membrane oxygenation
Emergency medical services
Emergency medical technician
European resuscitation council
European society of cardiology
European Society of Intensive Care Medicine
Fraction of inspired oxygen
False positive rate
Hospital Anxiety and Depression Scale
Heart and stroke foundation of Canada
Intra-aortic balloon pump
Inter-American Heart Foundation
Implantable cardioverter defibrillator
Intensive care unit
In-hospital cardiac arrest
International liaison committee on resuscitation
Ischemia reperfusion injury
Left bundle branch clock
Left ventricular assist device
Russian National Resuscitation Council
Systolic blood pressure
Central venous oxygenation
Systemic inflammatory response syndrome
Sequential organ failure assessment
Somatosensory evoked potentials
ST segment elevation
ST-elevation myocardial infarction
Targeted temperature management
Union of soviet socialist republics
World health organization
Withdrawal of life sustaining therapy
TOC z o “1-3” u hINTRODUCTION PAGEREF _Toc525457656 h 4CHAPTER 1:HISTORY OF EUROPEAN RESUSCITATION COUNCIL (ERC) PAGEREF _Toc525457657 h 61.1 The discovery of cardiopulmonary resuscitation (CPR) PAGEREF _Toc525457658 h 81.2 The discovery of defibrillation PAGEREF _Toc525457659 h 11CHAPTER 2:THE STRUCTURE OF ERC GUIDELINES FOR RESUSCITATION 2010 PAGEREF _Toc525457660 h 152.1 Adult advanced life support (ALS) according ERC Guidelines for resuscitation 2010 with focus on Post-Resuscitation Care PAGEREF _Toc525457661 h 15CHAPTER 3:THE STRUCTURE OF ERC GUIDELINES FOR RESUSCITATION 2015 PAGEREF _Toc525457662 h 193.1 Chain of survival PAGEREF _Toc525457663 h 193.2 Adult Basic Life Support (BLS) and Automated External Defibrillation (AED) PAGEREF _Toc525457664 h 213.3 Adult Advanced Life Support (ALS) PAGEREF _Toc525457665 h 23CHAPTER 4:POST-RESUSCITATION CARE IN ERC GUIDELINES 2015 PAGEREF _Toc525457666 h 264.1 Post-cardiac arrest syndrome (PCAS) PAGEREF _Toc525457667 h 274.1.1 Phases of Post-Cardiac Arrest Syndrome PAGEREF _Toc525457668 h 284.1.2 Pathophysiology and clinical picture of post-cardiac arrest syndrome PAGEREF _Toc525457669 h 294.2 Post-Resuscitation Care Algorithm PAGEREF _Toc525457670 h 344.2.1 Airway, breathing and circulation care after resuscitation PAGEREF _Toc525457671 h 354.2.2 Optimisation of neurological recovery after resuscitation PAGEREF _Toc525457672 h 414.2.3 Neurological prognostication in comatose survivors of cardiac arrest PAGEREF _Toc525457673 h 524.2.4 Rehabilitation of cardiac arrest survivors PAGEREF _Toc525457674 h 55CHAPTER 5:EVALUATION OF POST-RESUSCITATION CARE RELATED TO THE ERC GUIDELINES FOR RESUSCITATION 2015 PAGEREF _Toc525457675 h 56CHAPTER 6: THE STRUCTURE OF AMERICAN HEART ASSOCIATION (AHA) GUIDELINES FOR CARDIOPULMONARY RESUSCITAION (CPR) AND EMERGENCY CARDIOVASCULAR CARE (ECC) 2015 PAGEREF _Toc525457676 h 596.1 Comparison between the key issues of ERC Guidelines 2015 and AHA Guidelines 2015 for Post-Resuscitation Care PAGEREF _Toc525457677 h 59CONCLUSIONS PAGEREF _Toc525457678 h 62REFERENCES PAGEREF _Toc525457679 h 66APPENDIX PAGEREF _Toc525457680 h i
INTRODUCTIONCardiovascular diseases constitute a leading cause of death in the world, as 30% of the total global mortality or in other words, 17 million deaths per year are attributed to cardiovascular diseases. It is estimated that 40-50% of these cardiovascular deaths and approximately 500.000 deaths solely in Europe are caused by sudden cardiac arrest. The survival rate from these incidents is only 1% worldwide, thus the bystander cardiopulmonary resuscitation (CPR) is more valuable now than it has ever been. The proper approach of CPR can increase profoundly the survival rate by 2-3 times, which could save up to 100.000 lives per year in Europe. Thus, focusing on CPR and spreading the word about its importance must be a paramount priority in the field of medicine. Although the knowledge of CPR is enriched continuously due to its major role, not only in the life of healthcare professionals, but also in the life of educated in CPR bystanders, the care that the victim receives after the successful CPR is still well hidden behind the spotlight. The topic and aim of this diploma thesis is to focus on post-resuscitation care and its importance in improving the quality of life of cardiac arrest victims, always by following the European Resuscitation Council’s Guidelines of 2015.
The European Resuscitation Council’s Guidelines of 2015 are divided into eleven different sections and explain in detail the process of CPR. Section 1 is an executive summary of the guidelines, section 2 refers to the adult Basic Life Support (BLS) (1) and to Automated External Defibrillation (AED), section 3 includes the adult Advanced Life Support (ALS) (4), section 4 covers the cardiac arrest in special circumstances (2), section 5 introduces the guidelines for post-resuscitation (3), section 6 consists of pediatric life support (5), section 7 explains the resuscitation and support of babies at birth (6), section 8 refers to the initial management of acute coronary syndromes (7), section 9 includes first aid (8), section 10 covers the education and implementation of resuscitation and finally (9), section 11 introduces the ethics of resuscitation and end-of-life decisions (10). This diploma thesis refers to section 5 of the guidelines concerning post-resuscitation.
Since their creation in 2012, the European Resuscitation Council’s Guidelines are improved thoroughly in order to provide all the up-to-date information for better treatment of patients. The last Guidelines before 2015 are the ones from 2010 and thus, in every section of the new Guidelines exists a part named “Summary of changes since 2010 Guidelines”. There, all the changes between the old and new Guidelines are briefly explained in order to set the scenery for the reader for further explanation later. The aim of this thesis is to focus and explain more in detail the progress of the Guidelines throughout the years 2010 and 2015. The ultimate target remains section five of the Guidelines that focuses on Post-Resuscitation Care. The purpose of this thesis is to underline the paramount importance of Post-Resuscitation Care to faster healing of the patient, avoiding any complications that might worsen his/hers quality of life.
The diploma thesis is divided into chapters and sections in order to be more clear and understandable for the reader. More details about the chapters and the sections can be found in the contents. At the end of the diploma thesis, the reader can find the bibliography, containing all the references used for the elaboration of the thesis.
CHAPTER 1:HISTORY OF EUROPEAN RESUSCITATION COUNCIL (ERC)During the past century, there has been a great progress in cardiopulmonary resuscitation (CPR) and in general, in emergency medical care. In the year of 1960, modern CPR was introduced by Kouwenhoven, Jude and Knickerbocker, and by 1966 these techniques were adopted by the first CPR Conference of the American National Academy of Sciences. It was then recommended that all healthcare professionals should receive appropriate training in order to be able to respond in emergency situations in the most effective way and for the benefit of the patient. In 1967, the concept of Chain of Survival was introduced by Vladimir Negovsky, Peter Safar, and Fritz Ahnefeld and it is nowadays used universally.
The fourth CPR Conference was held in Dallas in 1985 and gave inspiration to numerous European scientists to create national CPR councils and working groups. The rapid scientific, political and economic development in Europe created the perfect time for an international collaboration, so in 1986, Lars Mogensen proposed the establishment of a working group on CPR in the European Society of Cardiology (ESC), as he was himself a well-distinguished cardiologist. In 1988, his proposal was rejected at the ESC Congress in Vienna; however he was not discouraged. He gathered, in the catering area of the congress, a group of enthusiasts including: Douglas Chamberlain, Leo Bossaert, Hugh Tunstall-Pedoe, Paul Hugenholtz, Stig Holmberg, and John Camm and all together they agreed to set up an interdisciplinary international collaborative European council on CPR, and chose the name ‘European Resuscitation Council’ (ERC).
On 13 December 1988, the first meeting of the 20 founding members of ERC took place in Antwerp (15). There, Douglas Chamberlain became temporary Chairman and Leo Bossaert temporary Secretary until official elections could take place. Eventually, in August 1989, an Executive Committee elected Peter Baskett as the first Chairman, with Stig Holmberg vice-chairman, Daniel Scheidegger as Honorary Treasurer and Leo Bossaert as Honorary Secretary. Peter Baskett was succeeded in turn by Wolfgang Dick, Pierre Carli, Petter Andreas Steen, David Zideman, Bernd Boettiger, and Maaret Castren.
The newly formed ERC set up formal collaborations with more than 30 National Resuscitation Councils (NRCs), both inside and outside of Europe. As the Organization kept growing, in 1991 the official journal of ERC, called Resuscitation, was created by Douglas Chamberlain as the first editor-in-chief (followed by Peter Baskett and Jerry Nolan).
In 1991, there was also a proposal for international cooperation from the American Heart Association. Eventually, the International Liaison Committee on Resuscitation (ILCOR) was established at the first Congress of ERC, which took place in Brighton in 1992. Nowadays, ILCOR includes (apart from the American Heart Association (AHA) and the European Resuscitation Council (ERC), the Heart and Stroke Foundation of Canada (HSFC), the Australian and New Zealand Committee on Resuscitation (ANZCOR), the Resuscitation Council of Southern Africa (RCSA), the Inter-American Heart Foundation (IAHF), and the Resuscitation Council of Asia (RCA).
In 1992, the first guidelines for the practice of CPR were created with the consensus of ILCOR, and since then, they are reviewed in intervals of approximately 5 years (16). In that notice, guidelines were created in 1998, 2000, 2005, 2010, 2015 and are accepted in most parts of Europe as the standard of care and the reference for clinical practice.
In 2012, a written declaration with recommendations to increase awareness of Cardiac Arrest in Europe was made by some ERC members and European Members of Parliament. As a result, a dedicated annual day to increase European Cardiac Arrest Awareness, named “European Restart a Heart Day”, was set on 16th October, starting in 2013. The progress continued in 2016, when the World Health Organization (WHO) in cooperation with the ERC, ILCOR, the European Patient Safety Foundation, and the World Federation of Societies of Anesthesiologists, shaped the program “Kids Save Lives”, which targets to train children in schools worldwide in the basics of CPR.
Despite of the ERC’s tremendous development through the years, its core goal remains the same as when the ERC was established back in 1988: ‘To save human life by improving standards of resuscitation in Europe, and by coordinating the activities of European organizations with a legitimate interest in cardiopulmonary resuscitation’.
1.1 The discovery of cardiopulmonary resuscitation (CPR)Cardiopulmonary resuscitation is defined as the manual application of chest compressions and ventilations to patients in cardiac arrest, done in an effort to preserve intact brain function until advanced help arrives and further measures are taken to restore spontaneous blood circulation (usually defibrillation and intravenous cardiac drugs). The concept of artificial respiration began in the 16th century with Vesalius’s research on living animals and continued on 18th century, when the Paris Academy of Sciences officially recommended mouth-to-mouth resuscitation for drowning victims in 1740.
In the discovery of CPR, a crucial role was played by Professor Vladimir Alexandrovich Negovsky, a Russian academic, founder of V.A. Negovsky scientific Research Institute of General Reanimatology of the Russian Academy of Medical Sciences, which itself was founded as a laboratory for resuscitation at the institute of neurosurgery, named “Restoration of life processes in near-death processes” in 1936.
Fig. SEQ Figure * ARABIC 1: Vladimir Alexandrovich Negovsky(Source: V.A. Negovsky Research Institute of General Reanimatology, Russian Academy of Medical Sciences)
In 1948, the laboratory was transformed into an independent structure of the Russian Academy of medical sciences and in 1985 it was transformed into the Institute of General Reanimatology of USSR Academy of medical sciences. The V.A. Negovsky scientific research institute of general reanimatology of the Russian academy of medical sciences created also the Russian National Resuscitation Council (RusNRC) in 2004. V.A. Negovsky was named the “father of reanimation” since in 1961, he proposed the new term “reanimaology” on the congress of trauma specialists in Budapest. He was an outstanding pathophysiologist who was listed among the greatest medical scientists of the 20th century along with Roentgen, Freud, Fleming. His innovative work in the field of reanimatology (intensive therapy) as an independent specialty and an important part of anesthesiology showed the way towards the amelioration of the field. His research into clinical death and resuscitation started during World War II in 1942 and continued after the war in the clinic of Professor A. Bakulev (1948-1956) and in the Botkin Hospital, where the first independent department of reanimatology was established on 1959. He created the term “post-resuscitation disease” which focuses on a specific pathophysiologic state of vital organ systems early after ischemic anoxia (13). V.A. Negovsky created international contacts and cooperated with the most prestigious scientists in the field of anesthesiology, such as P. Safar.
In 1767, the Society for the Recovery of Drowned Persons in Amsterdam became the first institution that dealt with sudden and unexpected death in an organized manner. They made recommendations on warming the drowned victim, on removing swallowed or aspirated water by positioning the victim’s head lower than feet, on applying manual pressure to the abdomen, on respiring into the victim’s mouth, on tickling the victim’s throat, on ‘stimulating’ the victim by means like rectal and oral fumigation with tobacco smoke and on bloodletting. The Society for the Recovery of Drowned Persons claimed to have saved 150 persons with their recommendations, only within four years of their founding.
In 1891, Dr. Friedrich Maass performed the first ever documented chest compression in humans, which gave the lead to Dr. George Crile, who reported the first successful external chest compressions in humans in 1903. In 1954, the anesthesiologist James Elam was the first to prove that expired air was sufficient to maintain adequate oxygenation and two years later, in 1956, he invented mouth-to-mouth resuscitation together with Peter Safar.
Fig. SEQ Figure * ARABIC 2: James Elam and Peter Safar(Source: Photographic archive of University of Chicago and University of Pittsburgh)
Safar conducted the research on existing basic life support procedures including controlling a person’s breathing airway by tilting back his/her head with an open mouth and using mouth-to-mouth breathing. He combined these with a procedure known as closed-chest cardiac massage and thus, he invented the basic life support method of CPR (12). Throughout his life Safar was hesitant to take credit for inventing CPR, since from his point of view, he brought to light effective procedures that humans had already discovered, and he put them together into what he called “the ABCs” – maintaining a patient’s Airway, Breathing and Circulation.
This revolutionary invention was used by the United States military to revive unresponsive victims in 1957 and by 1960, it was adopted by the National Academy of Science, American Society of Anesthesiologists, Medical Society of the State of New York and the American Red Cross. Programs were created by the American Red Cross in order to teach physicians and general public the principles of close-chest cardiac resuscitation and by 1963, the American Heart Association formally endorsed CPR. In 1972, Leonard Cobb organized the world’s first mass citizen training in CPR in Washington called Medic 2, where he helped in training over 100,000 people during the first two years of the program and by 1979, advanced cardiovascular life support (ACLS) is created. During 1980’s and more particular in 1981, a program to provide telephone instructions in CPR began in Washington and it used emergency dispatchers to give instant directions through the telephone while the fire department and EMT personnel were on their way to the scene. By 1988, pediatric BLS, pediatric ALS and neonatal resuscitation came to life.
1.2 The discovery of defibrillationDefibrillation is defined as the restoration of the rhythm of a fibrillating heart by electric shock (11). This life-saving procedure is focused on cardiac dysrhythmias and more specifically on ventricular fibrillation (VF) and non-perfusing ventricular tachycardia (VT). In 1849 the German scientist Carl Friedrich Wilhelm Ludwig and his student Moritz Hoffa became the first to document the onset of ventricular fibrillation, by inducing it in a dog’s heart with electric current applied directly to the ventricles. For many years, fibrillation was considered a phenomenon that had little relevance to human clinical situations, although it was a topic of some debate whether the heart could recover from fibrillation. Most physiologists believed that the uncontrollable contractions were caused by abnormal impulse generation and conduction within the network of nerve fibers. The Swiss physiologist Edmé Vulpian was the first to suggest the myogenic model of arrhythmia, thus showing the way to the research in the right direction. He was also responsible for the creation of the term fibrillation, in reference to the disorderly movements of the heart fibers, and described the event as a progression of distinct stages. The British physiologist John McWilliam confirmed Vulpian’s conclusions independently and suggested the great importance of ventricular fibrillation in human deaths. Between 1887 and 1889, McWilliam published a series of articles in the British Medical Journal, in which he distinguished between different types of sudden cardiac failure, and wrote the first classic, detailed description of fibrillation. The next breakthrough was made by a team of two physiologists, Jean Louis Prevost and Frederic Battelli, at the University of Geneva. In the 1899 issue of the Journal de Physiologie et de Pathologie Generale, Prevost and Battelli reported that it was possible to arrest heart contractions altogether by delivering a strong electric shock (2,400–4,800 V) to the body of an animal. Furthermore, they found that they could stop not only regular heart rhythm in this way, but also fibrillation induced by application of a weaker current a short time (15s) earlier. The electrodes were placed in the mouth and the small intestine of the animal, and the shock delivered for up to 1 s in duration. Thus, Prevost and Battelli performed the first true, internal defibrillation. Although Prevost and Battelli were experimenting with dogs and internal electrodes, another scientist, Louise Robinovitch, very nearly invented both the external pacemaker and the transthoracic defibrillator (14). Robinovitch found that existing methods of resuscitation took too long to set up while the patient was deprived of oxygen. She suggested using electrical current to induce both respiration and heartbeat without opening the chest cavity, and in fact designed a device that could be carried by an ambulance and plugged into the household electricity grid.
Due to lack of scientific understanding of the mechanism of fibrillation, it was not until the 1920s when the scientists started again the research on the matter. Funds were donated to various academic centers and laboratories, including Johns Hopkins University, where physicians Orthello Langworthy and Donald Hooker were working with engineering professor William Kouwenhoven and accidentally rediscovered defibrillation as well as what would eventually become CPR.
By the 1930s results were being published again, more promising than before. Hooker, Kouwenhoven, and Langworthy were initially unaware of Prevost and Battelli’s experiments. They began by placing the electrodes directly in the chest cavity of the dogs, against the myocardium of the ventricles. In 1933 they succeeded in arresting the fibrillation when they accidentally gave a second current application, hence the term countershock. Later they found out about the Prevost and Battelli papers and acknowledged them. When they pushed paddles hard against the chest to lower the impedance, they noticed an arterial pressure increase and thus also discovered chest compressions.
Meanwhile, former students of the earlier pioneers were continuing their work far from its places of origin. In the United States, Carl Wiggers was pursuing the line of investigation he began in his student days under his mentor, W.P. Lombard, who himself had been a student of Carl Ludwig. He set out to find out about the basic causes and mechanisms of fibrillation and the research definitely paid off. In 1940 Wiggers published a landmark paper, giving for the first time a mechanistic explanation for the induction of ventricular fibrillation, through the concept of the vulnerable period. According to the Wiggers-Wegria model, fibrillation can occur if a second heartbeat is initiated before the natural end of the preceding contraction is reached. This period coincides with the appearance of the T wave on the ECG. A distinctive property of the vulnerable period is such that it responds in the same fashion to stimulation of different sorts: fibrillation may result from artificial stimulation by electricity, or from more “natural” physiological triggers. However, Wiggers was quite skeptical on the subject of transthoracic defibrillation, believing that the risks of the method of applying 3,000 V at 25–30 A to a patient’s body can cause severe burns, disrupt the function of the central nervous system, and induce dangerous spasms in the respiratory system were too high. Also, he believed that the limited time (2–3 min after the beginning of fibrillation) during which defibrillation was useful, posed a problem, as it was difficult to produce a confident diagnosis in such short a time, and delivering a shock in the absence of a definitive diagnosis was unacceptably dangerous. Therefore, Wiggers’s recommendation was to use the electric defibrillation only in the operating room, for cases when the chest cavity was already opened and the electrodes could be placed directly on the heart. In such cases, current from the wall outlets would be sufficient to defibrillate, and direct heart massage could be used to reduce hypoxia and aid the resumption of heart contractions. Transthoracic defibrillation, it was clear, would wait for the coming of yet newer advances: the development of cardiopulmonary resuscitation, and the invention of a safer way to defibrillate.
During 1947, US surgeon Claude S. Beck is the first to save a human life through defibrillation, restoring his 14-year-old patient’s heart beat during a surgical procedure. By 1956, Kouwenhoven develops external defibrillators but during his experiments discovers and develops CPR. Harvard cardiologist Paul M. Zoll demonstrates the first closed chest (external) defibrillation and by 1960, Portable DC-powered defibrillators are developed by Harvard’s Bernard Lown and University of Washington’s K. William Edmark, allowing treatment outside hospitals for the first time. In Ireland of 1966, cardiologists J. Frank Pantridge and John S. Geddes are the first to install portable external defibrillators in an ambulance, creating the first mobile ICU. By 1978, the first Automated External Defibrillator (AED) is introduced, comprising sensors to detect in ventricular fibrillation, while the instructions are electronically provided, thus reducing the degree of training required to operate them.
Key factors in the boom in pacing and defibrillation research in the mid-twentieth century included an improved understanding of arrhythmias, experience with open-chest defibrillation, rising expertise in cardiac surgery, and a post–World War II cultural change that redefined the hospital as a technological center equipped and intended for the delivery of intensive care to critically ill patients. Finally, biomaterials and microcircuit electronics were vital in opening new possibilities for medical research and vice versa: refinement of life-saving devices provided a demand for the development and production of advanced power sources, insulation materials, circuit components, and technical support. Defibrillation not only fed off the boom of cardiology as a complex specialty after the 1970s, but itself contributed to the building of optimism and confidence about medical technology as the means to conquer heart disease.
CHAPTER 2:THE STRUCTURE OF ERC GUIDELINES FOR RESUSCITATION 2010
The ERC guidelines for resuscitation 2010 are divided into ten sections as mentioned below:
Adult basic life support and use of automated external defibrillators. (75)
Electrical therapies: automated external defibrillators, defibrillation, cardioversion and pacing. (76)
Adult advanced life support. (77)
Initial management of acute coronary syndromes. (78)
Paediatric life support. (79)
Resuscitation of babies at birth. (80)
Cardiac arrest in special circumstances: electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution. (81)
Principles of education in resuscitation. (82)
The ethics of resuscitation and end-of-life decisions. (83)
2.1 Adult advanced life support (ALS) according ERC Guidelines for resuscitation 2010 with focus on Post-Resuscitation CareAfter a brief look at the structure of ERC guidelines for resuscitation 2010, it is quite obvious that there is not any specific section in those guidelines, solely focused on post-resuscitation care of the patient. Back in 2010, post-resuscitation care was incorporated into the adult advanced life support (ALS) section of the guidelines.
The ALS section of the 2010 guidelines give greater emphasis on the techniques used and the reaction time spent after the recognition of an acute incident, thus making the recovery of the patient an easier process for everyone involved. It highlights the importance of minimally interrupted chest compressions and focuses on the “track-and-trigger” warning systems for identifying at-risk patients and treating them as soon as possible in order to prevent a possible in-hospital cardiac arrest. These systems help to raise awareness on the potential risk of sudden cardiac death not only in, but also out of the hospital, thus helping the healthcare professionals and the involved bystanders to be more prepared. As far as the tracheal intubation is concerned, its early placement is not required, unless it is achieved by highly trained individuals and without the interruption of the chest compressions for long periods of time. Delivery of drugs via a tracheal tube is no longer recommended and if intravenous (IV) access is not possible, drugs should be given by the intraosseous (IO) route. In order to be able to monitor continuously the tracheal tube placement, the quality of CPR and more importantly the indications of return of spontaneous circulation (ROSC), the role of capnography is thoroughly emphasized in the guidelines of 2010. The monitoring of oxygen saturation of arterial blood (SaO2) by pulse oximetry and/or arterial blood gas analysis is also crucial due to the fact that the hyperoxaemia (94-98%) caused after the ROSC, can be harmful to the patient.
In addition, the ALS section of 2010 guidelines gives a great emphasis on post-resuscitation care, leading the way for further improvement in the field of post-resuscitation. To begin with, post-cardiac arrest syndrome is brought to discussion more extensively as far as its early recognition and treatment are concerned. In those guidelines we can finally see some recognition of the importance of creating a specific post-resuscitation protocol with the sole target to improve the survival rate of cardiac arrest victims after ROSC. One of the most important parts, not only of the 2010 but also of the 2015 guidelines, is the highlighted importance of the use of primary percutaneous coronary intervention (PCI) in appropriate (including comatose) patients with sustained ROSC after cardiac arrest. As far as the glucose control in the same type of patients is concerned, blood glucose values >10 mmol l-1 (>180 mg dl l-1) must be treated but in the same time, hypoglycaemia must be avoided. Another important matter brought to the fore in these guidelines is the use of therapeutic hypothermia in comatose survivors of cardiac arrest, associated with both shockable and non-shockable rhythms, although not many evidence exist for use after cardiac arrest in patients with non-shockable rhythms. In case a comatose patient has been treated with therapeutic hypothermia after a cardiac arrest or in general in the case of surviving a cardiac arrest, the existing and widely accepted predictors of life expectancy that point towards a poor survival rate of the patient are considered now unreliable.
Attention to post-cardiac arrest syndrome
Creation of specific post-resuscitation protocol.
PCI in patients with sustained ROSC after cardiac arrest.
Glucose control – blood glucose values >10 mmol l-1 (>180 mg dl l-1) must be treated while avoiding hypoglycaemia.
Therapeutic hypothermia in patients with shockable and non-shockable rhythms.
Table 1: Overview of post-resuscitation care on ALS guidelines 2010 according ERC.
Last but not least, in the ALS guidelines of 2010 according to ERC, apart from the parts which refer to post-resuscitation care, we can also come though sections which refer to the importance of ultrasound imaging in ALS, as well as sections which refer to changes in the drugs that are being used in these acute circumstances. When talking about asystole or pulseless electrical activity (PEA), atropine is no longer recommended for routine use, and as far as ventricular fibrillation (VF)/ventricular tachycardia (VT) cardiac arrest is concerned, treatment includes 1mg of adrenaline after the third shock and once chest compressions have restarted. The treatment is then continued with 1mg of adrenaline every 3–5 min (during alternate cycles of CPR), while 300mg of amiodarone is also given after the third shock. This third shock is part of the three quick successive shocks which are used for VF/VT in the cardiac catheterisation laboratory or in the post-operative period after cardiac surgery.
Finally, the importance of precordial thump is diminished, while the importance of continuation of chest compressions during the charging of the defibrillator is being underlined due to the minimization of the pre-shock pause. Some older recommendations are also removed from the guidelines, including the previously specified period of CPR in cardiac arrest victims before out-of-hospital defibrillation without the presence of EMS personnel.
Fig. SEQ Figure * ARABIC 3: The ALS algorithm of ERC guidelines 2010(Source: Summary of the main changes in the Resuscitation Guidelines- ERC
summary booklet 2010-page 5)
CHAPTER 3:THE STRUCTURE OF ERC GUIDELINES FOR RESUSCITATION 2015The ERC guidelines for resuscitation 2015 are divided into eleven sections as mentioned below:
Adult basic life support and automated external defibrillation. (1)
Adult advanced life support. (4)
Cardiac arrest in special circumstances. (2)
Post-resuscitation care. (3)
Paediatric life support. (5)
Resuscitation and support of transition of babies at birth. (6)
Initial management of acute coronary syndromes. (7)
First aid. (8)
Principles of education in resuscitation. (9)
The ethics of resuscitation and end-of-life decisions. (10)
3.1 Chain of survivalBasic life support and the use of automated external defibrillation constitute the most important steps towards the successful resuscitation, thus their quality will certainly affect the recovery of the patient after the resuscitation. One of the most important mnemonics in medicine is the ABC of resuscitation, stating the first steps of BLS as: Airway-Breathing-Circulation. Following the ABC mnemonic and the chain of survival, and from the moment we suspect a cardiac arrest, the key observations are unresponsiveness and abnormal breathing. More specifically, the chain of survival includes:
Early recognition of the symptoms of myocardial ischaemia (e.g. chest pain) that will allow us to call immediately for help and prevent an upcoming cardiac arrest (84-86). Early recognition includes unresponsiveness and not breathing normally.
Early bystander CPR, which will provide us and the patient more time and will eventually multiply by 2-3 times the chances of survival (87-89). It is favorable if the bystander is trained in CPR, although not trained bystanders must be given instructions from the emergency medical dispatcher until professional help arrives (90-92).
Early defibrillation in order to restart the heart as soon as possible. “Early” implies 3-5 minutes after the collapse, in order to increase survival rates 50% – 70%. The early defibrillation can only be achieved if there is public access to AEDs (93,94,95). Each minute of delay decreases the chances of survival by 10% – 12%.
Early advanced life support and standardised post-resuscitation care with the purpose of restoring the patient’s quality of life if the resuscitation fails. This includes eliminating the etiological factors, as well as airway management and initiation of drug treatment.
Fig. SEQ Figure * ARABIC 4: The chain of survival (Source: ERC guidelines for resuscitation 2015, section 2)
3.2 Adult Basic Life Support (BLS) and Automated External Defibrillation (AED)33502604361815Fig.5: The BLS/AED Algorithm.
(Source: ERC guidelines for resuscitation 2015, section 2)
00Fig.5: The BLS/AED Algorithm.
(Source: ERC guidelines for resuscitation 2015, section 2)
33502604361815Fig. SEQ Figure * ARABIC 5: The BLS/AED AlgorithmFig. SEQ Figure * ARABIC 5: The BLS/AED Algorithm33502607620Adult basic life support begins with the unresponsiveness of the victim and his/hers abnormal breathing pattern. As soon as the cardiac arrest is recognized by a bystander or the emergency medical services (EMS), the initiation of CPR together with the use of AED is crucial. The basic mnemonic in BLS is “ABC”, which stands for Airway – Breathing – Circulation. Firstly, the airway management includes the opening of the airway using the head tilt and chin lift technique, while making sure that a foreign object is not blocking the airway. Secondly, the breathing is being assessed by observation of the chest movements. Normal breathing rates vary between 12-20 breaths per minute, so any breathing rate below 12 should lead the bystander or the EMS towards CPR. Last but not least, circulation is being assessed for its presence or absence by measuring the carotid pulse, although since 2010, the American Heart Association and the International Liaison Committee on Resuscitation have replaced the assessment of circulation with the chest compressions. The need to start directly with the chest compressions was born due to the difficulty in assessing the presence or absence of circulation, thus making clear that performing chest compressions on a beating heart causes less harm than not being able to perform them when the heart is not beating. The opinions differ and this is the reason why the American Heart Association is already using the mnemonic “CAB”, which stands for Chest compressions – Airway – Breathing.
Thus, after the bystander recognizes the cardiac arrest, he needs to make sure about his/hers personal and the safety of the victim. If the victim is unresponsive, the opening of the airway and the assessment of breathing follows. At that point, the emergency services should be alerted the AED should be found if available in the area. If one is not sure about the emergency phone number of his/hers country, the European emergency phone number 112 can be used free of charge from everywhere in Europe in order to contact the emergency services such as the ambulance, the police or the fire brigade. Chest compressions should be initiated at the lower half of the victim’s sternum (centre of the chest), in a depth of approximately 5cm-6cm and at a rate of 100-120 compressions per minute, while at the same time the chest should be allowed to recoil completely after each compression. After 30 chest compressions and with an open airway (head tilt – chin lift technique), 2 rescue breaths should be performed only by a trained individual, by gently sealing the victim’s nose and blowing air steadily into his/hers mouth for about 1 second, while observing whether the chest rises. If the chest fails to rise, the airway is not opened properly and the rescue breaths are not effective, thus the bystander must repeat the head tilt – chin lift technique. The time between the rescue breaths and the chest compressions should be limited to no more than 10 seconds. One cycle of CPR is made of 30 chest compressions and 2 rescue breaths (30:2), although if the bystander is untrained or unable to perform the rescue breaths, he/she must continue with chest compressions only CPR. If we take into consideration the 100-120 chest compressions per minute, we conclude that within 2 minutes, 5 cycles of CPR must be performed before the bystander swaps over and until professional medical help arrives. If the AED is available, it must be switched on and the electrode pads must be attached to the victim’s bare chest. The AED can be used in children older than 8 years old and it can be also performed by untrained individuals, since the AEDs provide clear instructions through screen indications and voice prompts. Once the electrode pads are attached to the victim, all rescuers should follow the auditory/visual directions, while ensuring that nobody is touching the victim’s body in order for the AED to analyze the rhythm. If a shockable rhythm is detected, a single shock is applied and as soon as the shock is delivered, the chest compressions should immediately resume, followed by the rescue breaths. After approximately 2 minutes of CPR, the AED re-analyses the rhythm and voice prompts will guide the rescuer to continue the procedure.
3.3 Adult Advanced Life Support (ALS)Advanced life support (ALS) consists of all the interventions that extend basic life support (BLS) in order to further support the circulation and breathing. The main components of BLS include chest compressions and rescue breaths, while ALS is focused on the monitoring of the electrical activity of the heart by a defibrillator/cardiac monitor.
Before the assessment of the heart rhythm and in between each cycle, 2 minutes of CPR are indicated, as well as the injection of 1mg adrenaline every 3-5 minutes until ROSC is achieved (22). As soon as the defibrillator is attached to the victim’s chest, an assessment between shockable (VF/pulseless VT) and non-shockable (PEA/asystole) rhythms occurs.
In case of non-shockable rhythms (VF/pulseless VT), the defibrillator is charged, chest compressions are interrupted and a shock is delivered (150J for biphasic waveforms). The delay between the pause of chest compressions and the delivery of the shock must be minimized in order to increase the chances of successful defibrillation (23-26). Immediately after the shock, CPR must continue for 2 minutes, starting with the 30 chest compressions in order to limit the post-shock pause and the total peri-shock pause (23,24). When the 2 minutes have passed, reassessment of the rhythm occurs, and if there is still VF/pulseless VT, a second shock is delivered (150J-360J for biphasic waveforms). Then, we repeat the same cycle: continual of CPR for 2 minutes-reassessment of the heart rhythm- if there is still VF/pulseless VT, delivery of a third shock (150J-360J for biphasic waveforms) -resume of CPR beginning with the chest compressions. If ROSC has not been achieved with this 3rd shock and if IV/IO access has been previously obtained, adrenaline 1 mg and amiodarone 300 mg should be administered during the next 2 min of CPR, although it is of paramount importance to administer the drugs without affecting the quality of CPR (27,28). If ROSC is suspected during CPR, the administration of adrenaline must stop, but if cardiac arrest is confirmed at the next rhythm check, the administration of adrenaline is necessary, as it can improve myocardial blood flow and increase the chance of successful defibrillation with the next shock. After each 2-min cycle of CPR, a rhythm check occurs. If the rhythm changes to non-shockable (PEA/asystole) and only if the rhythm is organised (complexes appear regular or narrow), we should try to feel a pulse. If there is any doubt about the presence of a pulse in the presence of an organised rhythm, we must immediately resume CPR. The ultimate goal remains the ROSC and then post-resuscitation care begins.
In case of shockable rhythms (PEA/asystole), the survival rate is diminished, thus it is harder for the EMS to reverse the situation. Pulseless electrical activity (PEA) is defined as a cardiac arrest with electrical activity of the heart (except ventricular tachyarrhythmia), which is usually associated with a palpable pulse (29). Once a PEA/asystole is detected by the AED, CPR should begin immediately, while extra attention should be paid, as the dispatcher should make sure that the leads are properly attached to the victim’s chest. We should continue the chest compressions even during ventilation through an advanced airway is being provided to the patient. After 2 minutes of CPR, we should reassess the rhythm and in case of redetection of PEA/asystole, we should continue with CPR. In case of an organised rhythm, we should try to palpate the pulse and if no pulse is found or if in doubt, we should resume the CPR. As in the case of non-shockable rhythms, after an IV/IO access is obtained, the administration of 1mg adrenaline is crucial, as well as the continuation of the CPR cycles. Then, we should reassess the pulse and if present, we should begin the post-resuscitation care. If signs of life are present during CPR, we should check the heart rhythm and the pulse. More particularly, if ROSC is suspected during CPR, the administration of adrenaline should stop and we should continue with the CPR. Then, we check once more the heart rhythm and if cardiac arrest is confirmed, we administer adrenaline. Moreover, if we are not sure whether the rhythm is PEA/asystole or extremely fine VF, we should continue chest compressions and ventilation without attempting defibrillation. Thus, the CPR can improve the amplitude and frequency of the VF and in that way, improve the chance of successful defibrillation (30-32). If the heart rhythm changes into VF, we continue with the algorithm of the shockable rhythms, and if not, we continue with CPR and administer adrenaline every 3–5 min if a palpable pulse is not detected.
Fig. SEQ Figure * ARABIC 6: The ALS algorithm of ERC guidelines 2015(Source: ERC guidelines for resuscitation 2015, section 1)
CHAPTER 4:POST-RESUSCITATION CARE IN ERC GUIDELINES 2015
When the ERC guidelines for resuscitation were published in 2015, post-resuscitation care won finally the place it deserved among the other sections of the guidelines, since in 2010, as previously mentioned, it was incorporated into ALS section of the guidelines. To achieve this major milestone, the ERC and the European Society of Intensive Care Medicine (ESICM) collaborated by creating this section into the guidelines in order to show the importance of high-quality post-resuscitation care in the survival of patients after acute incidents. Thus, these guidelines are being co-published in ERC and in Resuscitation and Intensive Care Medicine journal. The major changes since the guidelines of 2010 include:
The greater importance of urgent coronary catheterization and percutaneous coronary intervention (PCI) after out-of-hospital cardiac arrest due to a possibly cardiac cause.
The temperature management remains crucial and the targeted temperature is now 36? (instead of 32-34? that was previously recommended), while the prevention of fever remains very important.
Prognostication is performed by a multimodal strategy, with greater emphasis on allowing sufficient time for neurological recovery and for clearance of sedatives.
A new section has also been added about rehabilitation after survival from a cardiac arrest, which includes systematic organization of follow-up care, together with screening for potential cognitive and emotional impairments and provision of information.
The beginning of post-resuscitation phase occurs at the place of the cardiac arrest and right after the ROSC is achieved. As soon as the patient is stabilized, he/she is transferred to specialized high-care facility (for instance the emergency room or the intensive care unit (ICU)) for further monitoring and treatment. According to the quick response and the quality of CPR by the bystanders, the chances of immediate awaking, after cardiac arrest, range from 15-46% (41-43). If the patient is in a comatose state, he/she is admitted to the ICUs and as many as 40-50% of the patients survive and can be discharged from the hospital, depending on different parameters like the cause of cardiac arrest, the quality of care etc. (36,39,42-46). As far as the neurological outcome is concerned, most of these patients have a good prognosis with just subtle cognitive impairment (50-53). However, it is important to mention that in case of doubt for the patient’s neurological function after cardiac arrest, we should perform tracheal intubation and focus the treatment on improvement of hemodynamic, respiratory and metabolic variables, without forgetting the targeted temperature management.
4.1 Post-cardiac arrest syndrome (PCAS)Post- cardiac arrest syndrome (PCAS) is defined as the results of ischemia that occur in the body after a cardiac arrest, as well as the body’s response to CPR and the following successful resuscitation (21). It includes post-cardiac arrest brain injury, myocardial dysfunction, systemic ischemia/reperfusion response and the persistent precipitating pathology (21,54,55). Post-cardiac arrest syndrome does not necessarily occur and it may not occur at all if the cardiac arrest is of short duration. Although, if it occurs, the majority of patients will need multi organ support and treatment depending on the severity of the post-cardiac arrest syndrome, which is based on the cause and the duration of the cardiac arrest. The treatment which the patients receive during the post-resuscitation period influences drastically the overall outcome and particularly the quality of their neurological recovery (33-40).
As far as the post-cardiac arrest brain injury is concerned, it can manifest as myoclonus, seizures, coma, as well as different degrees of neurocognitive degeneration and in the worst case scenario, brain death. Brain injury is the most common cause of death among patients who survive the ICU admission, with the percentage of deaths rising up to 25% after in-hospital cardiac arrest and approximately 66% in out-of hospital cardiac arrest (56-59). Post-cardiac arrest brain injury causes the majority of later deaths.
On the other hand, cardiovascular failure/myocardial dysfunction causes most deaths in the first three days after the attack (56,59,60). In case of a bad prognosis, the most common cause of death rising up to half of the total number of patients suffering is withdrawal of life sustaining therapy (WLST) (43,59).
As it was mentioned before, the post-cardiac arrest syndrome also includes the systemic ischemia/reperfusion response, which activates the immune system and the coagulation pathways, thus contributing to multi organ failure and increasing the risk of infection (61-67). That is why the post-cardiac arrest syndrome shares numerous common features with sepsis, like vasodilation, abnormalities of microcirculation, endothelial injury and intravascular volume depletion (68-73).
4.1.1 Phases of Post-Cardiac Arrest SyndromeFor the purpose of easier understanding and treatment of post-cardiac arrest syndrome, we divide its course into 5 different phases:
Immediate post-arrest phase, which includes the first 20 min after ROSC.
Early post-arrest phase, which is between 20 min and 6-12 h after ROSC, when early interventions might be most effective.
Intermediate phase, which is between 6-12 and 72 h, when injury pathways are still active and aggressive treatment is typically instituted.
Recovery phase, which is the period after 3 days, when prognostication is more reliable.
Rehabilitation phase, which is the period after the recovery of the patient, when he/she regains lost skills and maximum self-sufficiency.
-2974975136525Figure SEQ Figure * ARABIC 7: Phases of post-cardiac arrest syndrome0Figure SEQ Figure * ARABIC 7: Phases of post-cardiac arrest syndrome
4.1.2 Pathophysiology and clinical picture of post-cardiac arrest syndromeThe increased mortality after a cardiac arrest and ROSC is highly depended on the pathophysiology of post-cardiac arrest syndrome and the fact that it affects multiple organs. The key components of post-cardiac arrest syndrome, as mentioned before, include:
Post-cardiac arrest brain injury.
Brain injury consists one of the most common causes of death after a cardiac arrest since the brain can tolerate ischaemia only for a short period of time. The pathophysiological mechanisms in post-cardiac arrest brain injury include: excitotoxicity, disrupted calcium homeostasis, free radical formation, pathological protease cascades, and activation of cell death signaling pathways (96-98). The above pathways occur hours to days after ROSC and in the same time period the degeneration of neuron subpopulations in the hippocampus, cortex, cerebellum, corpus striatum, and thalamus happens (99-103). In addition, if the cardiac arrest was prolonged, fixed and/or dynamic failure of cerebral microcirculatory reperfusion despite adequate cerebral perfusion pressure (CPP) can follow (104,105), which will eventually lead to persistent ischaemia and small infarctions in the brain. Except from this cerebral microcirculatory failure, macroscopic reperfusion is often hyperaemic in the first few minutes after cardiac arrest because of elevated CPP and impaired cerebrovascular autoregulation (106-107). In that way, the hyperaemic reperfusion can worsen the brain oedema and lead to reperfusion injury of the brain. Cerebral oxygen delivery can, apart from reperfusion, also be compromised by hypotension, hypoxaemia, impaired cerebrovascular autoregulation, and brain oedema. Other factors that can impact brain injury and increase the risk of brain death after cardiac arrest include: pyrexia (;39 °C in the first 72 h) (108), hyperglycaemia (associated with poor neurological outcome) (41,109-114), and seizures (worsen the total prognosis). Post-cardiac arrest brain injury is usually manifested by: coma, seizures, myoclonus, varying degrees of neurocognitive dysfunction (from memory deficits to persistent vegetative state/ disorders of arousal and awareness), and even brain death (115-123).
Post-cardiac arrest myocardial dysfunction.
Post-cardiac arrest myocardial dysfunction can be detected within 30 minutes after ROSC by monitoring of ejection fraction (decreases from 55% to 20%) and left ventricular end-diastolic pressure (increases from 8-10 to 20-22 mmHg) (124,125). Three major pathways contribute to the pathophysiology of post-cardiac arrest myocardial dysfunction including cardiovascular ischemia reperfusion injury (IRI), catecholamine-induced myocardial injury, and cytokine-mediated cardiovascular dysfunction (17). Its pathophysiology overlaps with the pathophysiology of myocardial dysfunction (developing as a result of IRI seen after cardiopulmonary bypass), cytokine excess (seen in sepsis), and catecholamine toxicity (as in stress-induced cardiomyopathy). During the period of myocardial dysfunction, coronary blood flow is not reduced, thus the situation is reversible and recovery is expected within 24-48h if there is no previous cardiac history (125). Echocardiography is the primary tool for diagnosing post-cardiac arrest myocardial dysfunction, although invasive hemodynamic monitoring can also be used in patients after ROSC. In general, the treatment is focused on optimising preload, restoring arterial pressure and increasing the contractility to ensure proper tissue perfusion. Inotropic drugs like dobutamine infusions of 5-10 ?g kg?1 min?1 can be very helpful since they improve systolic (left ventricular ejection fraction) and diastolic (isovolumic relaxation of left ventricle) dysfunction after cardiac arrest (124). We can conclude that post-cardiac arrest myocardial dysfunction is a multifactorial syndrome which arises from the interaction between pre-arrest cardiac pathology and intra-arrest cardiac insults. It can develop in up to 2/3 of patients after a cardiac arrest, even in the absence of prior cardiac disease, and this is the reason why physicians should emphasize more to its recognition and treatment in the clinical praxis.
Systemic ischaemia/reperfusion response.
Ischaemia contributes to the pathophysiology of many conditions faced by anesthesiologists, including myocardial infarction, peripheral vascular insufficiency, stroke, and hypovolemic shock. Although restoration of blood flow to an ischemic organ is essential to prevent irreversible cellular injury, reperfusion can cause cellular damage to previously viable ischemic tissues, which is defined as ischemia/reperfusion injury (IRI). During cardiac arrest, delivery of oxygen and metabolic substrates is ceased and we can partially reverse the situation with CPR, because cardiac output and systemic oxygen delivery (DO2) values are still less than normal after CPR. This occurs due to the fact that during CPR, a compensatory increase in systemic oxygen extraction occurs, which leads to decreased central (ScvO2) or mixed venous oxygen saturation (126). Even after ROSC, tissue oxygen delivery is not enough because of myocardial dysfunction, press or dependent haemodynamic instability and microcirculatory failure. The lack of oxygen will eventually cause endothelial activation and systemic inflammation (127), in cases like thrombolytic therapy, organ transplantation, coronary angioplasty, aortic cross-clamping or cardiopulmonary bypass (128,129). If severe enough, the inflammatory response after IRI may result in the systemic inflammatory response syndrome (SIRS) or multiple organ dysfunction syndrome (MODS), attacking also non-ischemic organs, which will eventually lead to death. The clinical manifestations of IRI are diverse and range from transient reperfusion arrhythmias to the development of fatal MODS, as previously mentioned. Although the response to IRI varies greatly among individuals, the presence of risk factors such as hypercholesterolemia, hypertension, or diabetes contributes to a worse prognosis.
Clinically, IRI can result in four types of injury, including myocardial stunning, the no-reflow phenomenon, reperfusion arrhythmia, and lethal reperfusion injury. Myocardial stunning is defined as a condition of persistent mechanical dysfunction after opening an occluded blood vessel, regardless of the absence of irreversible damage, which can last up to two weeks until complete recovery. In the clinical setting, myocardial stunning can be diagnosed using various image modalities such as dobutamine echocardiography, myocardial contrast echocardiography etc.. In addition, no-reflow phenomenon is defined as an incomplete and uneven reperfusion on microvascular level, even though the proximal artery has been re-opened after a period of ischemia. This phenomenon occurs in patients after PCI and increases their mortality rate. It is caused from endothelial damage, leukocyte plugging and mechanical compression, while hyperglycemia is also associated with it. Another type of injury that results from IRI is reperfusion arrhythmias occurring in up to 80% of patients after acute myocardial infarction within 48h of the incident. The most common arrhythmias that might occur after PCI include: accelerated idioventricular rhythm, sinus bradycardia, nonsustained ventricular tachycardia and sinus tachycardia, but some life-threatening arrhythmias suck as ventricular tachycardia (VT) and ventricular fibrillation (VF) can also occur. Last but not least, lethal reperfusion injury can occur after IRI and is defined as myocardial injury caused by the restoration of coronary blood flow after an ischemic episode. It can cause immediate cardiomyocyte death at the beginning of reperfusion and this is the reason why it is the most serious consequence of IRI, preventing the recovery of the ischemic myocardium after reperfusion therapy. We can conclude that systemic ischaemia/reperfusion response apart from impaired oxygen delivery and utilisation, can lead to intravascular volume depletion, impaired vasoregulation and increased susceptibility to infection and according to the type of injury it will cause, it can define the mortality of a patient.
Persistent precipitating pathology.
The pathophysiology of post-cardiac arrest syndrome is commonly complicated by persisting acute pathology that caused or contributed to the cardiac arrest itself. Pathologies such as acute coronary syndrome (ACS), pulmonary diseases (e.g. pulmonary embolism), haemorrhage and haemorrhagic cardia arrest, sepsis, and various toxidromes can worsen post-cardiac arrest syndrome. More specifically, ACS occurs in 40% of patients after cardiac arrest, which is calculated by elevations in troponin T measured during treatment (130). In addition, troponin T measurements can help in the diagnosis of acute myocardial infarction (AMI) 12h after ROSC (131). As far as thromboembolic diseases are concerned, pulmonary embolism can also be caused after cardiac arrest and can be fatal for the patient. We can also add to the precipitating pathology haemorrhagic cardiac arrest, primary pulmonary diseases like chronic obstructive pulmonary disease (COPD), asthma, or pneumonia, sepsis, acute respiratory distress syndrome (ARDS) and multiple organ failure. Other precipitating causes of cardiac arrest may require specific treatment during the post-cardiac arrest period. These include drug overdose and intoxication that need to be treated with specific antidotes, and environmental causes such as hypothermia which requires active temperature control, or oxygen free radicals.
Table 2: Post-cardiac arrest syndrome: pathophysiology, clinical manifestations, and potential treatments.
4.2 Post-Resuscitation Care Algorithm18649951057275The goal of all ERC guidelines throughout the years is the easy accessibility and their wide use in clinical practice. Based on these principles, and specifically in our case, the post-resuscitation care algorithm has been created for the return of spontaneous circulation (ROSC) and quick follow-up care of the patient after resuscitation. It is divided into 3 different segments:
Immediate treatment, which includes control of airway/breathing, circulation and temperature.
Diagnosis, which takes into consideration whether or not the incident is due to a cardiac cause, while recommending diagnostic tools according to each case.
Optimization of recovery, which refers to ICU management, secondary prevention, as well as follow-up and rehabilitation.
-6794517145Fig. SEQ Figure * ARABIC 8: Post-resuscitation care algorithm. Return of spontaneous circulation and comatose0Fig. SEQ Figure * ARABIC 8: Post-resuscitation care algorithm. Return of spontaneous circulation and comatose(Source: ERC guidelines for resuscitation 2015, section 5)
4.2.1 Airway, breathing and circulation care after resuscitationExtra attention should be given on this part of the guidelines, since airway, breathing and circulation constitute the most important steps towards a full recovery of a patient after a cardiac arrest. If the patient is treated directly after a cardiac arrest, the chances of achieving an immediate return of cerebral function are increased. In this case, and if arterial blood oxygen saturation is less than 94%, oxygen should be administered via facemask. Failure of proper oxygenation can lead to hypoxaemia and hypercarbia, which will eventually increase the chances of a later cardiac arrest or secondary brain injury. On the other side, according to animal studies, if hyperoxaemia occurs early after ROSC, it can cause oxidative stress and harm to the post-ischaemic neurons (132). It was also proved that if an arterial oxygen saturation of 94-96% in the first hour after ROSC (controlled reoxygenation) is achieved, it has better neurological outcomes than achieving oxygen saturation of 100% (133). Thus, we conclude that in case of oxygen saturation reaching 100% after ROSC in first 24h (post-resuscitation hyperoxaemia), the neurological outcome is worse than in the cases of normoxaemia or hypoxaemia (134). In order to avoid hyperoxaemia, we should adjust the fraction of inspired oxygen (FiO2) to produce an arterial oxygen saturation of 94-96%.
Ventilation control, tracheal intubation and sedation are really important steps in a patient after cardiac arrest and with problems in cerebral function. In general, hypocardia induced by hyperventilation constricts the cerebral vessels and thus causes decreased blood flow in the brain, which will eventually lead to cerebral ischaemia (135,136). According to some observational studies, from one hand, hypocapnia causes poor neurological outcome in a patient after cardiac arrest, and on the other hand mild hypercapnia has a better neurological prognosis (137). Taking into consideration the above-mentioned data, we conclude that normocardia is the ultimate goal to achieve by adjusting accordingly the ventilation and by monitoring it using the end-tidal CO2 and arterial blood gas values. Protective lung ventilation has not been studied extensively, although it is known that is can possibly cause hypercapnia, which as mentioned before, can harm the post-cardiac arrest patient. This is the reason why protective lung strategy is applied on those patients with recommendations on tidal volume of 6-8 ml kg-1 (ideal body weight) to prevent hypercapnia and on end expiratory pressure of 4-8cm (73). Another recommendation includes the insertion of a gastric tube to decrease distention of the stomach (caused by mouth-to-mouth and bag-mask ventilation), which splints the diaphragm and creates problems breathing. In order to reduce the oxygen consumption, the administration of sedatives is also recommended. Some evidence also support the infusions of neuromuscular blocking drugs in post-cardiac arrest patients because continuous neuromuscular blockade can decrease their mortality (138). On the other hand, the data are not sufficient and these infusions can create difficulties in the clinical examination and mask some epileptic episodes. This is the reason why continuous EEG is recommended for the detection of seizures, especially when neuromuscular blockade infusions are used (139). Last but not least, a chest radiograph is crucial in order to detect any probable complications from CPR (e.g. rib fracture associated pneumothorax) (140), to search for pulmonary oedema, and to make sure about the proper positioning of the tracheal and gastric tubes, as well as of the central venous lines.
Administration of O2 with facemask (if arterial SaO2 ; 94%).
Adjustment of FiO2 to produce SaO2 of 94-96%.
Normocardia must be achieved with adjustment and monitoring of ventilation using end-tidal CO2 and arterial blood gas values.
Protective lung strategy in patients with tidal volume of 6-8 ml kg-1 (to prevent hypercapnia) and end expiratory pressure of 4-8cm.
Release of stomach tension by inserting gastric.
Administration of sedative to reduce O2 consumption.
Infusions of neuromuscular blocking drugs (low quality data).
Continuous EEG monitoring for detection of seizures.
Table 3: Overview of airway and breathing recommendations in ERC guidelines for post-resuscitation care 2015.
Moving on to the blood circulation, coronary artery disease and more specifically acute coronary syndrome (ACS) is one major cause of out-of-hospital cardiac arrest (OHCA) (141). Thus, according to different studies, patients with ROSC after a cardiac arrest are suitable for percutaneous coronary intervention (PCI) (142). PCI after ROSC is also associated with patients who have ST-elevation myocardial infarction (STEMI) (39). In more than 80% of patients with ST segment elevation (STE) or left bundle branch block (LBBB) in their ECG after ROSC, we can find an acute coronary lesion (143) and this is the reason why, an early PCI is recommended, especially in patients with STE. This early intervention will also help towards a more favorable neurological result and in general, increase the survival rate of the patient. Other studies also prove that favorable results come from combining PCI with targeted temperature management (TTM), and especially with therapeutic hypothermia (144). The mortality rate dropped drastically from 66% to 25% in a study with 40 comatose post-cardiac arrest patients who were treated without therapeutic hypothermia and with therapeutic hypothermia respectively (39). In this study, not only the total prognosis was improved by using TTM, but also the neurological outcome of the patients. We should also emphasize the proper timing for the interventions needed and more particularly in the case of STEMI, PCI should be performed immediately, while in NSTEMI it should be done in less than 2 hours after the cardiac arrest, depending also on the haemodynamic instability (145). This approach of performing PCI in patients without an obvious non-coronary cause of their cardiac arrest (because there are limitations on ECG-based diagnosis) is not widely accepted and this is the reason why more experts agree on the PCI on patients depending on the increased risk of them having a coronary cause for their cardiac arrest. This risk usually depends on factors like patient’s age, haemodyamic instability, duration of CPR, neurological status on arrival at the hospital, presence of cardiac rhythm and in general the perception of possible cardiac etiology. Taking into account all these evidence, physicians can decide whether PCI is needed acutely after ROSC or whether they can delay it. To summarise, immediate coronary angiography is considered in all post-cardiac arrest patients with ACS suspicion, while coronary angiography with subsequent PCI if indicated is definite in post-cardiac arrest patients with ECG criteria for STEMI. In case PCI is not available, we can consider thrombolytic therapy as an alternative for post-cardiac arrest management of STEMI.
As mentioned before, what actually create a discussion between experts are the non-cardiac causes of OHCA, since those are the ones that have not been researched extensively like the cardiac causes. This is the point where monitoring steps in to give a solution. Monitoring plays a crucial role in identifying the causes of a cardiac arrest, as well as in the treatment of patients. It is divided into three categories including general intensive care monitoring, more advanced haemodynamic monitoring, and cerebral monitoring. General intensive care monitoring includes: arterial catheter, oxygen saturation by pulse oximetry, continuous ECG, CVP, ScvO2, temperature (bladder, esophagus), urine output, arterial blood gases, serum lactate, blood glucose, electrolytes, CBC, and general blood sampling and chest radiograph. Advanced haemodynamic monitoring includes: echocardiography and cardiac output monitoring and cerebral monitoring includes: EEG for seizure detection and CT/MRI. Early identification of the causes of a cardiac arrest, especially if they are non-cardiac such as respiratory or neurological causes help the patient receive optimal care in a more specialized setting like the ICU and deepens the knowledge of the physicians on his/hers prognosis so they can personalize even more the treatment. We can say in certainty that a brain and chest computed tomography scan (CT scan) when the patient is admitted to the hospital is very important in identifying the respiratory or neurological causes of a cardiac arrest as soon as possible. The guidelines state that in case of no neurological or respiratory signs or symptoms (e.g. seizures, shortness of breath etc.) or if there is no clinical evidence or ECG-based diagnosis for myocardial ischaemia, the first step is coronary angiography followed by a CT scan if no causative lesions are found. Following these guidelines, it is easier to discover the cause of the cardiac arrest, thus providing better healthcare to the patient.
Another extremely important matter constitutes the haemodynamic management after a cardiac arrest, since haemodynamic instability is very common after these acute incidents. In between the manifestations of haemodynamic instability we find hypotension, arrhythmias and decreased cardiac index (146), which are mainly caused by mechanisms like intravascular volume depletion, impaired vasoregulation and myocardial dysfunction. In the case of myocardial infarction we need to figure out its severity by echocardiography (147) and as far as the treatment is concerned, inotropics such as dobutamine are used (148) except from when systematic inflammatory response occurs after a cardiac arrest. In this case, we also need to treat the severe vasodilatation and vasoplegia that are caused by the systemic inflammatory response (146) by administering noradrenaline with or without dobutamine, as well as fluids. If the combination of inotropics, vasoactive drugs and fluid resuscitation does not work and the patient’s circulation cannot stabilize, we should consider the use of a mechanical circulatory assistance device (e.g. IMPELLA) (35,149). As far as the monitoring is concerned, echocardiography is recommended, as well as the measurements of BP (arterial line for continuous measurements in ICU), HR, urine output, plasma lactate clearance rate and central venous oxygen saturation. In addition, a great number of studies are trying to figure out the optimal targets for mean arterial pressure (MAP) after a cardiac arrest, but there is not a definite conclusion yet. One study in particular shows the good neurological outcome if the time-weighted average MAP (measured every 15 minutes) is greater than 70mmHg (150), without knowing if the administration of vasoactive medication in order to achieve this target actually has a better neurological outcome. Considering all the above, and if no other data are available, we should target for a MAP that help us achieve an adequate urine output (1ml kg-1 h-1) and physiological or decreased plasma lactate values. In this action plan, we should also take into consideration that the target MAP depends on the individual and may vary depending on his/hers comorbidities, normal BP values, cause of cardiac arrest and severity of myocardial dysfunction (20). When talking about BP, we should not forget to mention the effects of tachycardia and bradycardia after a cardiac arrest. According to studies, tachycardia was associated with a bad outcome (151), and while at the beginning bradycardia below 40 min-1 was also considered harmful, more recent retrospective studies have shown that bradycardia is associated with a favorable outcome (152). This type of bradycardia can be left without a treatment in case BP, lactate, ScvO2 and urine output are sufficient. Apart from the above, we also find out that after a cardiac arrest, an adrenal insufficiency appears and if accompanied by post-resuscitation shock, it is also associated with a bad prognosis (153). Studies have shown that IHCA had a positive outcome if treated with a combination of methylprednisolone and vasopressin with adrenaline, while treatment with steroids alone has not been studied yet and until further data appear, the administration of steroids alone is not recommended (154). Immediately after a cardiac arrest we should also expect a period of hyperkalaemia followed by hypokalaemia due to endogenous catecholamine release and correction of metabolic and respiratory acidosis that promote transportation of potassium into the cells. In the case of hypokalaemia we should administer potassium, setting as a goal the serum potassium concentration to be between the values of 4.0 and 4.5 mmol l-1, in order to avoid any ventricular arrhythmias that might be caused. If a ventricular arrhythmia is caused either way later than 24-48h after a cardiac arrest in ischaemic patients with left ventricular dysfunction, we should consider the insertion of implantable cardioverter defibrillator (ICD) (155). Moreover, ICDs can help patients after a cardiac arrest with structural heart diseases and inherited cardiomyopathies fight their risk of sudden death (secondary prevention) and thus decreasing their mortality (156).Either way, the insertion of an ICD should be performed after a specialized electrophysiological evaluation.
Immediate coronary angiography in all post-cardiac arrest patients after ROSC with ACS suspicion, while coronary angiography with subsequent PCI if indicated in post-cardiac arrest patients with ECG criteria for STEMI. In case PCI is not available, we can consider thrombolytic therapy.
TTM, especially with therapeutic hypothermia.
CT scan on admission.
Echocardiography for investigation of haemodynamic instability in myocardial infarction. In this case, treatment includes inotropics such as dobutamine.
In case of SIRS after a cardiac arrest, treatment includes administration of noradrenaline with or without dobutamine, as well as fluid resuscitation.
If the combination of inotropics, vasoactive drugs and fluid resuscitation does not work, we should consider the use of a mechanical circulatory assistance device such as IMPELLA.
Monitoring includes: echocardiography, BP measurement (arterial line for continuous measurements in ICU), HR, urine output, plasma lactate clearance rate and ScvO2.
MAP target value should help us achieve an adequate urine output (1ml kg-1 h-1) and physiological or decreased plasma lactate values.
Bradycardia below 40 min-1 can be left untreated in case BP, lactate, SvO2 and urine output are sufficient.
Relative adrenal insufficiency after IHCA should betreated with a combination of methylprednisolone and vasopressin with adrenaline, while treatment with steroids alone is not recommended.
Administration of potassium in order to reach the range of 4.1 – 4.5 mmol l-1, if hypokalaemia occurrs immediately after cardiac arrest.
Insertion of ICD, if a ventricular arrhythmia is caused later than 24-48h after a cardiac arrest in ischaemic patients with left ventricular dysfunction.
Table 4: Overview of circulation recommendations in ERC guidelines for post-resuscitation care 2015.
4.2.2 Optimisation of neurological recovery after resuscitationThe cerebral perfusion, after a cardiac arrest and ROSC, is affected variably according to animal studies. In the beginning after ROSC, we observe multifocal cerebral no-reflow followed by 15-30 minutes of global cerebral hyperaemia (157). After that and for the rest 24 hours, we can observe cerebral hypoperfusion, while simultaneously the cerebral metabolic rate of oxygen recovers. On the other hand and while sometimes brain oedema can occur after ROSC, we do not find increased intracranial pressure in these patients (158). We need to emphasize that for some time after a cardiac arrest, the autoregulation of cerebral blood flow is impaired in a great number of patients (35%), which proves that cerebral perfusion varies based on cerebral perfusion pressure (159). According to a study, the majority of these patients had increased BP before the cardiac arrest (160) which proves correct the guidelines of 2010 that recommended maintaining the MAP near patient’s normal values after ROSC (77).
A great chapter in post resuscitation care constitutes the sedation after a cardiac arrest since the data still vary considerably. Physicians usually sedate and ventilate patients for at least 24h after ROSC, although there are no sufficient evidence to support a defined duration for ventilation, sedation and neuromuscular blockade. What is certain about the duration of sedation and ventilation is that it is definitely depended on the patient’s specific treatment. When the treatment is focused on targeted temperature management (TTM), adequate sedation is needed, although it decreases the oxygen consumption, which is further reduced with therapeutic hypothermia. During induction of therapeutic hypothermia, maintenance, and rewarming and in order to reach the targeted temperature faster, adequate sedation is particularly important. There is no sufficient evidence to prove whether the choice of sedative influences the post-cardiac arrest outcome, but in most cases a combination of opioids (analgesia) and hypnotics (e.g. propofol or benzodiazepines) is administered. Short-acting drugs like propofol enable a more reliable and fast neurological assessment. If shivering occurs despite deep sedation, neuromuscular blocking drugs (as an intravenous bolus or infusion) should be used, while close monitoring of sedation and neurological signs such as seizures is crucial. To sum up, critically ill post-cardiac arrest patients need sedation for mechanical ventilation and therapeutic hypothermia. In addition, sedation scales can be extremely useful for monitoring purposes. Neuromuscular blockade can help the induction of therapeutic hypothermia, but if continuous infusions of neuromuscular blocking drugs become necessary, continuous EEG monitoring should be considered.
When talking about neurological recovery after a cardiac arrest we should underline that seizures occur in 10-40% of patients who remain comatose after ROSC, with myoclonus being the most common (18-25%) (161). The origin of these seizures is not always epileptic and this is the reason why intermittent electroencephalography (EEG) is necessary for distinction between epileptic and non-epileptic seizures. On the other hand, if a patient is diagnosed with status epilepticus, continuous EEG is needed in order to monitor the effects of the treatment. Patients with status epilepticus do not always have seizure manifestations in their clinical picture, since they can be masked with the use of sedation. Either way, it is not proved whether systematic detection and treatment of electrographic epileptic activity improves the neurological outcome of patients. Seizures increase cerebral metabolism up to 3 times (162) and can even worsen any brain injury that the cardiac arrest might have caused. The recommended treatment includes sodium valproate, levetiracetam, phenytoin (effective only in animal models) (163), benzodiazepines (e.g.clonazepam), propofol (better for post-anoxic myoclonus) or a barbiturate. Clonazepam is the most effective antimyoclonic drug, but sodium valproate and levetiracetam may also be effective (164). As far as the use of anticonvulsant drugs as prophylaxis after cardiac arrest in adults is concerned, there are not enough studies to support their use (165,166). Myoclonus and electrographic seizure activity, including status epilepticus can be related to a good neurological outcome after a cardiac arrest, but they also have a poor prognosis (167). To summarise, if seizures are prolonged, they can cause cerebral injury and this is the reason why they should be treated quickly and effectively with benzodiazepines, phenytoin, sodium valproate, propofol, or a barbiturate. These drugs can cause hypotension, and this must be also treated appropriately. Clonazepam is the drug of choice for the treatment of myoclonus and maintenance therapy should be administered after the first epileptic episode, once potential precipitating causes (e.g. intracranial haemorrhage, electrolyte imbalance) are excluded. Prospective studies are needed in order to determine the benefit of continuous EEG monitoring.
In order to optimise the neurological recovery we should definitely mention the glucose control after resuscitation, since increased blood glucose after a cardiac arrest and ROSC is associated with poor neurological outcome (168). Based on a randomized controlled trial, we find that the results of tight blood glucose control (4.4-6.1 mmol l-1 or 80-110 mg dl-1) with insulin are different in the surgical ICU and in the medical ICU. More specifically, in the surgical ICU, the mortality was decreased (169) and the peripheral and central nervous system were protected from the insulin use (170). On the other hand, in the medical ICU there was no difference in the mortality rate with the use of tight blood glucose control (171). In addition, when the patients were hospitalized in the ICU for three days or more, the mortality rate dropped from 52.5% to 43% with intensive insulin therapy. Increased mortality in ICU patients is also associated with severe hypoglycaemia (172) that sometimes even goes unnoticed in comatose patients. Moreover, hyperglycaemia is common in patients after a cardiac arrest and this is the reason why monitoring of glucose concentrations is essential. Based on the data from recent studies, treatment includes insulin infusions after ROSC, with targeted blood glucose at ?10 mmol l-1 (180 mg dl-1) and with simultaneous avoidance of hypoglycaemia (173) by not implementing strict glucose control after cardiac arrest.
The most important subject in optimisation of neurological recovery constitutes temperature control after cardiac arrest and this is the reason why a great part of the guidelines is dedicated to it. To begin with, it is proved that in the first 48h after cardiac arrest a great number of patients pass through a period of hyperthermia (hyperpyrexia) (174), and according several different studies hyperpyrexia after cardiac arrest is associated with poor neurological outcome (175,176). It is also proven that hyperthermia can occur after a period of mild induced hypothermia, called rebound hyperthermia, which increases the mortality rate and worsens the neurological outcome of post-cardiac arrest patients (177-179). As far as the treatment of pyrexia (?37.6°C) is concerned, there are no randomised controlled trials which evaluate its effect in comparison to no temperature control trials and many assume that the increased temperature can solely constitute an effect after a severely injured brain. Despite the fact that the effects of hyperthermia after cardiac arrest are not proven by clinical trials, physicians find reasonable to treat it by antipyretics and even to consider active cooling in unconscious patients.
In the subject of targeted temperature management and according to studies based on animals and humans, it is proven that mild induced hypothermia is a promising neuroprotective and cardioprotective treatment, while it helps to improve the state of the patient after a period of global cerebral hypoxia-ischaemia (180-182). The pathways that lead to cell death, including apoptosis (programmed cell death) are suppressed via cooling, while hypothermia also reduces the release of excitatory amino acids and free radicals by decreasing the cerebral metabolic rate of oxygen (CMRO2) by about 6% for each 1°C reduction in core temperature (180,183). In addition, hypothermia blocks the consequences of excitotoxin exposure inside the cell (high calcium and high concentrations of glutamate) and decreases the inflammatory response associated with the post-cardiac arrest syndrome. However, according to a recent study, the inflammatory cytokine response does not change in adult patients in the temperature range 33-36 °C (184). It is essential to mention that all studies of mild induced hypothermia after a cardiac arrest consist only of patients in coma. For instance, one randomized trial and one pseudo-randomised trial showed the improved neurological outcome in comatose patients after an out-of-hospital VF cardiac arrest, when they were discharged from the hospital or 6 months later (185,186). In these trials, the physicians started with cooling within minutes to hours after ROSC and the temperature was maintained between 32-34°C for 12-24h. On the other side, there are studies that did not show any improved neurological outcome with the use of targeted temperature management. For example, three cohort studies with a total of 1034 patients made a comparison between mild induced hypothermia (32-34°C) and no temperature management in OHCA and found no difference as far as the neurological outcome is concerned (187-189). Another retrospective cohort study including 8316 in-hospital cardiac arrest (IHCA) patients showed also no difference in the survival after hospital discharge among the patients who got treated with mild induced hypothermia and those who did not receive any temperature management (even though relatively few patients were treated with mild induced hypothermia) (191). Some studies, not only do not recommend mild induced hypothermia after cardiac arrest, but prove that its use has poor neurological outcome on patients. In particular, a retrospective registry study of 1830 patients showed an increase in poor neurological outcome among those with nonshockable OHCA treated with mild induced hypothermia (190). Although there are numerous studies before and after the implementation of targeted temperature management (TTM) in the case of IHCA, it is extremely difficult to interpret these data due to the fact that other changes also occur in the same time after a cardiac arrest. In other studies, TTM AT 33°C was associated with decreased heart rate, increased lactate, the need for increased vasopressor support and a higher extended cardiovascular sequential organ failure assessment (SOFA) score in comparison with TTM at 36°C (192). As far as the decreased heart rate (bradycardia) during mild induced hypothermia is concerned, many support that it can be beneficial for the patient since the autonomic function is probably preserved and that helps towards a good neurological outcome among comatose survivors of OHCA (193). Apart from the heart rate, a matter of discussion constitutes the optimal duration for TTM and mild induced hypothermia and although it is still unknown, most physicians are using 24h. Past trials were using TTM for 12-28h (185,186) and two observational trials found no difference in poor neurological outcome and mortality when comparing 24h to 72h of hypothermia (194,195).
Even though the term therapeutic hypothermia is widely used, nowadays the preferred term is targeted temperature management (TTM) or temperature control as mentioned before. The International Liaison Committee on Resuscitation and more specifically its Advanced Life Support Task Force created some recommendations on TTM (196) which are included on the ERC guidelines. To summarise these recommendations include:
Target temperature between 32-36°C for patients in whom temperature control is used.
Further research is needed to figure out whether some post-cardiac arrest patients are benefited from lower (32-34°C) or higher (36°C) temperatures.
TTM is recommended in patients after OHCA and ROSC, who remain unresponsive and have an initial shockable rhythm.
TTM is recommended in patients after OHCA and ROSC, who remain unresponsive and have an initial non-shockable rhythm.
TTM is recommended in patients after IHCA and ROSC, who have any initial rhythm.
In case TTM is used, the optimal duration for its use is at least 24h.
Although all the above are included in the ERC guidelines, it is underlined that not all the suggestions are strongly recommended since there are not enough evidence to support their use. Strong recommendations only exist for suggestions number 1. and 3., while the evidence are of moderate and low quality respectively. Suggestions number 4. , 5. and 6. are weakly recommended and the already existed evidence are of very-low quality. Thus, we can conclude with certainty that the optimal TTM after a cardiac arrest is not discovered yet and more high-quality evidence are needed, based on large trials and studies in order to figure out the optimal targeted temperature for these patients.
Apart from the optimal target temperature after cardiac arrest, there is also a big discussion around the optimal timing and more precisely, when to begin with the active temperature control. In the past, the recommendations suggested to start with cooling as soon as possible after the ROSC, but there are not sufficient evidence to support them, due to the fact that these recommendations were only based on preclinical data (182). In addition, investigations on animal data showed that earlier cooling after ROSC has better outcomes (197). Observational studies on this matter also exist and show that the patients who cool spontaneously faster after ROSC have a worse neurological outcome (198-200). Some hypotheses are also made and claim that patients with severe neurological injuries can lose more easily their ability to control body temperature, although these hypotheses have not been further investigated. A great number of trials exist and they support different times in temperature control after cardiac arrest. Five randomized control trials started with TTM directly after ROSC with cold intravenous fluids (201-204), one trial started with TTM during resuscitation also with cold intravenous fluids (205) and another trial started with TTM during the cardiac arrest using intranasal cooling (206). The volume of the cold fluid used was between 20 to 30 ml kg-1 and up to 2l, even though some patients did not receive the full amount of fluids before arriving at the hospital. The above-mentioned trials concluded that there was no difference in the patients’ mortality and neurological outcome whether they were given cold fluids or not. Due to the high significance of TTM after cardiac arrest, even more trials took place viewing the subject from different aspect each time. For example, four randomized controlled trials (RCTs) showed low quality evidence in support of an augmented risk of a reoccurring cardiac arrest if the patients received prehospital induced hypothermia (201,202,204). Some other trials were focusing on the incidence of pulmonary oedema in patients with and without post-cardiac arrest TTM. Most of them showed no difference whether or not TTM was used (201,205) and only one showed an increased incidence of pulmonary oedema in patients who received prehospital cooling (204). The conclusion from all these evidence is that prehospital cooling with rapid infusions of large volumes of cold intravenous fluid immediately after ROSC is not recommended. Some exceptions may be found in the case of well monitored patients whose target temperature is set lower (e.g. 33°C) and it still remains unknown whether some particular patients (e.g. patients whose transport to the hospital will take a long time) can benefit from early prehospital cooling. Apart from the early cooling strategies of rapid infusion of large volumes of cold intravenous fluid and prehospital cooling during CPR, there are no other strategies that have been thoroughly studied in the field of post-resuscitation care.
Maintenance of the MAP near patient’s normal values after ROSC.
Sedation and ventilation depending on the patient’s specific treatment (therapeutic hypothermia), usually by administering a combination of opioids (analgesia) and hypnotics (e.g. propofol or benzodiazepines).
Neuromuscular blocking drugs (IV or infusion) should be used if shivering occurs despite deep sedation, while close monitoring of sedation and neurological signs (e.g. seizures) is crucial. Continuous EEG monitoring should be considered if continuous infusions of neuromuscular blocking drugs are used.
Intermittent EEG for distinction between epileptic and non-epileptic seizures.
Continuous EEG to monitor the effects of treatment in patients with status epilepticus.
Treatment of seizures includes benzodiazepines (e.g.clonazepam), sodium valproate, levetiracetam, phenytoin, propofol (better for post-anoxic myoclonus) or a barbiturate. These drugs can cause hypotension, and this must be also treated appropriately.
Clonazepam is used for the treatment of myoclonus and maintenance therapy should be administered after the first epileptic episode, after potential precipitating causes (e.g. intracranial haemorrhage, electrolyte imbalance) are excluded.
Glucose control includes insulin infusions after ROSC, with targeted blood glucose at ?10 mmol l-1 (180 mg dl-1) and with simultaneous avoidance of hypoglycaemia by not implementing strict glucose control (4.4-6.1 mmol l-1 or 80-110 mg dl-1) after cardiac arrest.
TTM with mild induced hypothermia between 32-36°C in patients after OHCA and ROSC, who remain unresponsive and have shockable rhythm is strongly recommended. TTM in patients with an initial rhythm, or non-shockable rhythm, as well as the recommendation for the duration of TTM for at least 24h are still investigated.
Prehospital cooling with rapid infusions of large volumes of cold intravenous fluid immediately after ROSC is not recommended.
Table 5: Overview of optimization of neurological recovery recommendations in ERC guidelines for post-resuscitation care 2015.
We have already mentioned the topics of optimal target temperature and optimal timing to start with TTM, but the most important subject to mention is the actual procedure and practical application of TTM. To begin with, we need to underline that TTM is divided into three phases including induction, maintenance and rewarming (207). As far as induction and maintenance are concerned, external and/or internal cooling are being used. Rewarming is usually done spontaneously when the patient arrives at the hospital after a cardiac arrest, with temperature less than 36°C and the target temperature is 36°C. We have to emphasize that the maintenance phase does not change according to different target temperatures since for example; shivering is the same whether the patient is treated at 33°C or at 36°C (59). Although, if the target temperature is set at 36°C, it makes sense that the rewarming process will be shorter.
At this point, we need to precise the exact methods used for inducing and/or maintaining TTM, so external and/or internal cooling are achieved by using:
Ice packs and/or wet towels: are cost-effective but time consuming, can lead to temperature fluctuations and do not enable controlled rewarming (39,47,186). Ice cold fluids cannot be used to maintain hypothermia (208), but when used together with simple ice packs, they might have an adequate result (209).
Cooling blankets or pads (210,211,214,215).
Water or air circulating blankets (35,36,38,212,213).
Water circulating gel-coated pads (35,214,215).
Transnasal evaporative cooling (206): permits cooling before ROSC and is being investigated in a randomized controlled trial (216).
Intravascular heat exchanger: placed in femoral or subclavian veins (35,36,212,215).
Extracorporeal circulation: includes for example cardiopulmonary bypass) (217,218).
In the majority of cases, patients cool easily after ROSC because the temperature normally decreases either way within the first hour (41,175). When patients are admitted to the hospital after OHCA, their temperature ranges between 35°C and 36°C and according to a large trial, the average temperature was 35.3°C (59). If the target temperature is set at 36°C, patients are allowed to rewarm spontaneously and if the target temperature is set at 33°C cooling is facilitated by neuromuscular blockade and sedation, which will eventually prevent shivering (219). In order to reduce shivering, we can also use magnesium sulphate, a naturally occurring N-methyl-D-aspartate (NMDA) receptor antagonist (207,220). Some of the above-mentioned methods of maintaining TTM cause temperature fluctuations, which generally need to be avoided in order to achieve the proper temperature easily. This is the reason why external or internal cooling devices are used, which also provide continuous monitoring of the patient’s temperature (221). The most frequently used cooling and monitoring device is a thermistor placed in the patient’s bladder and/or oesophagus (207,222). It is not proven whether some cooling techniques have better results in comparison to others, or whether they increase the survival rate, but some data exist to prove that internal cooling devices provide more precise temperature control compared with external cooling techniques (215,221). The third phase of practical application of TTM is rewarming. During this phase, we observe changes in plasma electrolyte concentrations, effective intravascular volume and metabolic rate, which also occurs during cooling. The optimal rate of rewarming is not precisely set yet, although the rate of 0.25-0.5°C per hour is widely accepted (212). It is crucial to mention that rewarming should be achieved slowly due to the fact that rebound hypothermia can occur, which is associated with worse neurological outcome (177,178). In order to reduce this risk, the chosen target temperature must be 36 °C (59).
As far as temperature control is concerned, we figured out that cooling physiologically occurs after ROSC and this is the reason why the physiological effects, as well as the side effects of hypothermia must be monitored and managed properly (207). These effects include:
Shivering: increases metabolic rate and heat production, thus reducing cooling rates. It constitutes a physiological response and when it occurs in post-cardiac arrest patients with mild induced hypothermia, it helps towards a good neurological prognosis (223,224). In order to reduce shivering, apart from the above-mentioned techniques, we can also use sedation.
Increased systemic vascular resistance and arrhythmias: can be caused by mild induced hypothermia (225). The most frequent arrhythmia caused is bradycardia, which can be beneficial for the patient since it reduces diastolic dysfunction (226) and is associated with a good neurological outcome (152,193).
Diuresis and electrolyte abnormalities: such as hypophosphataemia, hypokalaemia, hypomagnesaemia and hypocalcaemia can also be cause by mild induced hypothermia (59,207,227).
Hyperglycaemia: caused by decreased insulin sensitivity and insulin secretion, which are in turn caused by hypothermia (186). In these cases treatment should include glucose control with insulin.
Increased bleeding: caused by impaired coagulation due to mild induced hypothermia. This side effect is not confirmed by clinical studies (35,59,185) since it is occurring rarely (228).
Increased infection rates: due to impaired immune system caused by mild induced hypothermia (207,229,230). In most cases, the infection is associated with pneumonia (231,232), but it does not affect the overall state of the patient. Prophylactic antibiotics are being used and eventually decrease the incidence of pneumonia, even though their use in such cases has not been thoroughly studied (233).
Increased serum amylase concentration: occurs during hypothermia, but its impact and importance have not been studied.
Reduced clearance of sedative drugs and neuromuscular blockers: by up to 30% at a core temperature of 34°C (234). If we want to keep the clearance at a normal level, a temperature closer to 37°C must be used.
In the subject of physiological effects and side effects of hypothermia, we also need to underline the contraindications of TTM. When the target temperature is at 33°C, the contraindications include severe systemic infection and pre-existing medical coagulopathy, while fibrinolytic therapy is not a contraindication of mild induced hypothermia.
Furthermore, mild induced hypothermia can be combined with neuroprotective drugs like Coenzyme Q10 (235), thiopental (165), glucocorticoids (154,236), nimodipine (237,238), lidoflazine (239) and diazepam (166), although these drugs can also be used alone. Until now there is not sufficient proof for their neurological benefit in post-cardiac arrest patients. Another therapy which is under investigation with a feasibility trial is the combination of mild induced hypothermia and xenon (240).
4.2.3 Neurological prognostication in comatose survivors of cardiac arrestTo begin with, the matter of prognostication is extremely sensitive in post-cardiac arrest patients since a wrong neurological prognosis can lead to false medical decisions. It is widely known that 2/3 of patients who die in the ICU after OHCA die from a neurological injury, such as hypoxic-ischaemic brain injury (241). These deaths are caused by active withdrawal of life sustaining treatment (WLST) after the responsible physicians made a prognosis of poor neurological outcome of the patient (55,58) and this is the reason why it is of paramount importance to minimise the risk of a false prediction. Ideally, in the prediction of a poor neurological outcome the false positive rate (FPR) should be zero with the narrowest possible confidence interval (CI). We should not forget that the therapy itself (e.g. TTM, sedation etc.) can interfere with the prognostication strategy (242) and in these cases prolonged observation of clinical signs more than 72h after ROSC is recommended.
The indicators on which the prognostication is based on can be found through clinical examination, electrophysiology, electroencephalography (EEG), presence of status epilepticus, presence of burst-suppression, biomarkers, neuron-specific enolase (NSE) threshold and imaging (brain CT and MRI). After specifying all the above, a suggested prognostication strategy is created in order to minimize the risk of wrong predictions on the neurological outcome of post-cardiac arrest patients.
To begin with, a poor outcome is predicted when there is bilateral absence of pupillary light reflex and/or corneal reflex at 72h after ROSC in the clinical examination, with FPR close to 0% whether the patient is treated with TTM or not (242,243,244). In addition, there is high FPR and increased sensitivity for prediction of poor outcome in patients with absent or extensor motor response to pain at 72h after ROSC and with or without TTM treatment (242,245). A poor neurological outcome was also associated with the presence of myoclonus (sudden, brief, involuntary jerks caused by muscular contractions or inhibitions) starting within 48h after ROSC in patients with or without TTM treatment (246,247). As far as electrophysiology is concerned, it is proven that bilateral absence of the N20 short-latency somatosensory evoked potentials (SSEPs) in post-cardiac arrest comatose patients, not treated with TTM, is a predictor of death or vegetative state with 0% FPR in 24h after ROSC (248). In patients treated with TTM, the bilateral absence of the N20 SSEP wave constitutes also a predictor of poor outcome during mild induced hypothermia (249) and rewarming (249,250,251). Electroencephalography (EEG) can also help to predict a poor neurological outcome when there is absence of EEG reactivity. In TTM-treated patients, poor outcome can be predicted with 2% FPR (252,253) during TH and with 0% FPR (252) after rewarming in 48-72h after ROSC. Another predictor of poor outcome can be the presence of status epilepticus in TTM-treated patients during TH or immediately after rewarming (254). Moreover, burst impression which consists of more than 50% of the EEG record with periods of EEG voltage <10?V with alternating bursts (255). In prognostication studies, burst-impression is usually a transient finding whether or not the patients are treated or not with TTM. During the first 24-48 h after ROSC (256) in non-TTM-treated patients or during hypothermia in TTM-treated patients (257) burst suppression may be compatible with neurological recovery while at ?72 h from ROSC (139,248) a persisting burst-suppression pattern is consistently associated with poor outcome. Some protein biomarkers such as NSE and S-100B may be also associated with poor neurological outcome. They are released after injury to neurons and glial cells respectively and their values in blood after cardiac arrest are associated with the extent of anoxic-ischaemic neurological injury. In addition, NSE threshold differs in TTM and non-TTM treated patients. In the first, the NSE threshold for prediction of poor outcome with 0% FPR at days 24-72 from ROSC was 33 mcg l-1 or less in some other studies (258,259). The main reasons for this variability in NSE thresholds include the use of heterogeneous measurement techniques (variation between different analysers) (260), the presence of extra-neuronal sources of biomarkers (haemolysis and neuroendocrine tumours) (261) and the incomplete knowledge of the kinetics of its blood concentrations in the first few days after ROSC. Last but not least, imaging is a great predictor of neurological outcome after a cardiac arrest. In the brain CT of a post-cardiac arrest patient with a global anoxic-ischaemic cerebral insult we can find cerebral oedema (262). On the other hand, on the MRI of the same kind of patient after global-ischaemic brain injury we can find hyperintensity in cortical areas or basal ganglia on diffusion weighted imaging (DWI) 1968503433445007042158212798(Source: ERC guidelines for resuscitation 2015, section 5)
020000(Source: ERC guidelines for resuscitation 2015, section 5)
749307971155Fig. SEQ Figure * ARABIC 9: Prognostication strategy algorithmFig. SEQ Figure * ARABIC 9: Prognostication strategy algorithmsequences.
4.2.4 Rehabilitation of cardiac arrest survivorsWhen the physicians follow the guidelines for post-cardiac arrest patients, the neurological outcome is favorable for the majority of patients and the rehabilitation must take place. It is common for the cardiac arrest survivors to face cognitive and emotional problems, as well as fatigue, which in particular can occur many years after the cardiac arrest and affects 56% of the survivors (51,266). As far as the cognitive problems are concerned, most of the patients face memory problems associated with attention and executive functioning (51,263). Long-term cognitive impairment affects half of the cardiac arrest survivors and even though they can be severe, they are mostly of mild form (50). On the other side, emotional problems also occur and they may include depression, anxiety and posttraumatic stress (264,265). All the above can interfere with the cardiac arrest survivor’s daily functioning and quality of life (265) and this is the reason why follow-up care after the hospital discharge is crucial. Follow-up care can be provided by a physician or a specialised nurse and must include at least:
Screening for cognitive impairments: Even though a gold standard does not exist in performing this type of screening, it is recommended to ask the patient and a relative or a caregiver about the presence of any cognitive complaints and follow-up the patient accordingly or refer him/her to a neuropsychologist for neuropsychological assessment or to a specialist in rehabilitation medicine for a rehabilitation programme (267). If possible, administer a structured interview or checklist, like the Checklist Cognition and Emotion (268) or a short cognitive screening instrument, such as the Montreal Cognitive Assessment (MoCA).
Screening for emotional problems: In this type of screening it is again recommended to ask the patient whether he/she experiences any emotional problems (e.g. symptoms of depression). For further investigation we can also use the Hospital Anxiety and Depression Scale (HADS) and the Impact of Event Scale (269,270). In the case of presence of emotional problems, we should refer the patient to psychologist or psychiatrist (271).
Provision of information: It is recommended to provide the patient with all the information concerning the potential non-cardiac consequences of the cardiac arrest he/she experienced, including cognitive impairment, emotional problems and fatigue.
CHAPTER 5:EVALUATION OF POST-RESUSCITATION CARE RELATED TO THE ERC GUIDELINES FOR RESUSCITATION 2015Evaluation of post-resuscitation care is based on the quality of life that it will be able to provide the cardiac arrest survivor. The quality of life of a patient after a cardiac arrest can be measured with different scales such as Glasgow Outcome Scale (GOS) and Cerebral Performance Category (CPC) scale, as well as psychological tests. To begin with, GOS is defined as a scale for patients with brain injuries (e.g. cerebral traumas) which categorizes the outcomes of patients who suffer traumatic brain injury and tries to figure out the objective degree of their recovery. Post-cardiac arrest patients can have severe neurological injuries due to decreased brain oxygenation and this is the reason why GOS can be applied on this type of patients. The GOS is a five-level score which includes:
Death: Severe injury or death without recovery of consciousness.
Persistent vegetative state: Severe damage with prolonged state of unresponsiveness and a lack of higher mental functions, meaning patient exhibits no obvious cortical function.
Severe disability: Severe injury with permanent need for daily support due to mental and/or physical disability (conscious but disabled).
Moderate disability: No need for assistance in everyday life, patient is independent as far as daily life is concerned (disabled but independent). The disabilities he/she might have include varying degrees of dysphasia, hemiparesis, or ataxia, as well as intellectual and memory deficits and personality changes.
Good recovery/Low disability: Patient can resume his/hers normal activities even though there may be minor neurological or psychological deficits.
Figure SEQ Figure * ARABIC 10: Glasgow Outcome Scale (GOS)(Source: Jennett B, Bond M. “Assessment of outcome after severe brain damage.” Lancet 1975 Mar 1;1(7905):480-4)
GOS can help the physicians predict the long-term course of rehabilitation, and categorize the quality of life that a patient will have after a cardiac arrest. In addition to GOS, Cerebral Performance Category (CPC) scale is being used, which basically categorizes the patients according to their neurological outcome after cardiac arrest. The “labeling” of patients in different categories with the use of CPC scale will eventually help evaluate the post-resuscitation care that the patient received after cardiac arrest. The CPC scale is a five segment scale (272) including:
CPC 1 – Good cerebral performance (normal life): The patient is alert, able to work and lead a normal life, even though some minor psychological or neurological deficits (e.g. mild dysphasia, nonincapacitating hemiparesis, minor cranial nerve abnormalities etc.) may occur.
CPC 2 – Moderate cerebral disability (disabled but independent): The patient is conscious with sufficient cerebral function for independent activities of daily life (e.g. dress, food preparation etc.) and for work in sheltered environment. Some other deficits such as hemiplegia, seizures, ataxia, dysarthria, dysphasia or permanent memory or mental changes can also occur.
CPC 3 – Severe cerebral disability (conscious but disabled and dependent): The patient depends on others for daily support because of impaired brain function, which can range from ambulatory state to severe dementia or paralysis. In this category we find patients such as the ones with paralysis who can communicate only with their eyes (locked-in syndrome).
CPC 4 – Coma or vegetative state (unconscious): The patient is unaware of his/hers surroundings even if he/she appears awake (vegetative state), has no cognition and no verbal or psychological interaction with the environment. In this category belongs any degree of coma without the presence of all brain death criteria. Patients can also have spontaneous eye opening and sleep/awake cycles even though they are cerebrally unresponsive.
CPC 5 – Brain death: The patient is certified brain dead or dead by additional criteria with apnea, areflexia, EEG silence etc..
CHAPTER 6: THE STRUCTURE OF AMERICAN HEART ASSOCIATION (AHA) GUIDELINES FOR CARDIOPULMONARY RESUSCITAION (CPR) AND EMERGENCY CARDIOVASCULAR CARE (ECC) 2015
The AHA guidelines for CPR and ECC were published on October 15, 2015 and consist of fourteen sections as mentioned below:
Evidence evaluation and management of conflicts of interest.
Systems of care and continuous quality improvement (CQI).
Adult basic life support (BLS) and cardiopulmonary resuscitation (CPR) quality.
Alternative techniques and ancillary devices for cardiopulmonary resuscitation (CPR).
Adult advanced cardiovascular life support (ACLS).
Post-cardiac arrest care.
Acute coronary syndromes (ACS).
Special circumstances of resuscitation.
Pediatric basic life support (PBLS) and cardiopulmonary resuscitation (CPR) quality.
Pediatric advanced life support (ALS).
6.1 Comparison between the key issues of ERC Guidelines 2015 and AHA Guidelines 2015 for Post-Resuscitation care
ERC guidelines 2015 for post-resuscitation care AHA guidelines 2015 for post resuscitation care
There is a greater emphasis on the need for urgent coronary catheterisation and percutaneous coronary intervention (PCI) following out-of-hospital cardiac arrest of likely cardiac cause. Emergency coronary angiography is recommended for all patients with ST elevation and for hemodynamically or electrically unstable patients without ST elevation for whom a cardiovascular lesion is suspected.
Targeted temperature management remains important but there is now an option to target a temperature of 36°C instead of the previously recommended 32–34°C. The prevention of fever remains very important. TTM recommendations have been updated with new evidence suggesting that a range of temperatures may be acceptable to target in the post–cardiac arrest period. After TTM is complete, fever may develop. While there are conflicting observational data about the harm of fever after TTM, the prevention of fever is considered benign and therefore is reasonable to pursue.
Prognostication is now undertaken using a multimodal strategy and there is emphasis on allowing sufficient time for neurological recovery and to enable sedatives to be cleared. Prognostication is now recommended no sooner than 72 hours after the completion of TTM; for those who do not have TTM, prognostication is not recommended any sooner than 72 hours after ROSC.
A novel section has been added which addresses rehabilitation after survival from a cardiac arrest. Recommendations include the systematic organisation of follow-up care, which should include screening for potential cognitive and emotional impairments and provision of information. Identification and correction of hypotension is recommended in the immediate post–cardiac arrest period.
All patients who progress to brain death or circulatory death after initial cardiac arrest should be considered potential organ donors.
Table 6: Comparison of key points of ERC and AHA Guidelines 2015 for post-resuscitation care.
(Source: ERC guidelines summary booklet 2015 – pages 4 and 5, AHA guidelines highlights 2015 – page 15)
From the table above, it is quite obvious that the ERC and AHA guidelines for post-resuscitation care of 2015 share many similarities. By reading the guidelines one can conclude that they are complementary to each other. It is logical that they are quite similar, since they are both focused on proper care of patients after a cardiac arrest and some differences that are present are mainly due to minor differences in values used in Europe and United States of America. The difference between the values that are being used occurs due to the fact that the overall health of the populations between each continent differs according environmental factors such as air pollution, nutrition etc..
CONCLUSIONSThe creation of guidelines is a continuous and time-consuming process and in case frequent changes to guidelines occur, they will create confusion, which could impair skill performance of healthcare providers and adversely impact patients’ outcomes. Nevertheless, if new and important data emerge, they must be implemented on daily clinical praxis for patients’ benefit. This is the reason why ERC has decided to keep on publishing new guidelines in five-year cycles. Even though we need to wait until 2020 to find out about the new guidelines on resuscitation, a lot of progress has been made since their last creation in 2015, since the scale and pace of new clinical trials and observational studies in resuscitation science has grown exponentially. ERC published an update of 2015 guidelines for resuscitation on November 2017 developed by the International liaison committee on resuscitation (ILCOR). All possible changes to ERC guidelines and their timescale for implementation are mentioned in the table below. High priority implementation will lead to active updates to course materials and dissemination of important changes, while routine implementation will be updated during the training material updates in 2020.
From table 7 (Summary of ILCOR CoSTR and ERC Guidelines 2017), we conclude that the up-to-date changes focus on six domains of the guidelines including: Dispatcher assisted CPR (273), Bystander delivered CPR (274), Emergency Medical Services (EMS) delivered CPR (275), compression to ventilation ratio (275), in-hospital resuscitation (276), and paediatric resuscitation (277).
After a thorough investigation of the ERC guidelines 2015 on post-resuscitation care, it is obvious that the treatment which a cardiac arrest survivor receives is crucial for his/hers quick rehabilitation and return to his/hers daily habits.
Apart from the ultimate goal to save the patient’s life, physicians must pay more attention on their handlings of patients after resuscitation. It is well-known that in such acute incidents, physicians work under extreme pressure to bring back to life the patient, but the same effort must be put also after the patient has been resuscitated.
-525145-72834500Table 7: Summary of ILCOR CoSTR and ERC Guidelines 2017
(Source: G.D. Perkins et al. / Resuscitation 123 (2018) 43-10)
The work of the physician must end after the patient is discharged from the hospital with the best possible prognosis, which is focused on the patient being able to resume the activities of his/hers daily life, and if possible without any disability. The reason why guidelines exist in every field of medicine is to provide physicians with clear instructions on how to handle acute and chronic incidents based on scientific research and clinical studies. The importance of the guidelines lies upon the fact that physicians are able to work more efficiently, since they have an in-depth reassurance of every step they need to follow in order to proper care for their patients. We also need to emphasise the role of the physician as an active healthcare provider, because even if the guidelines provide most of the information needed to treat post-cardiac arrest patients, the physician is the one that knows the exact history of his/hers patients and based on his/hers experience, he/she is able to make the right decisions for the patients’ final treatment plan.
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APPENDIX?. Step by step sequence of actions for use by the BLS/AED trained provider to treat the adult cardiac arrest victim. (Image source: ERC guidelines for resuscitation 2015, section 2)
LIST OF FIGURES
TOC h z c “Figure” Fig. 1: Vladimir Alexandrovich Negovsky PAGEREF _Toc525548315 h 8Fig. 2: James Elam and Peter Safar PAGEREF _Toc525548316 h 10Fig. 3: The ALS algorithm of ERC guidelines 2010 PAGEREF _Toc525548317 h 18Fig. 4: The chain of survival PAGEREF _Toc525548318 h 20Fig. 5: The BLS/AED Algorithm PAGEREF _Toc525548319 h 21Fig. 6: The ALS algorithm of ERC guidelines 2015 PAGEREF _Toc525548320 h 25Figure 7: Phases of post-cardiac arrest syndrome PAGEREF _Toc525548321 h 28Fig. 8: Post-resuscitation care algorithm. Return of spontaneous circulation and comatose PAGEREF _Toc525548322 h 34Fig. 9: Prognostication strategy algorithm PAGEREF _Toc525548323 h 54Figure 10: Glasgow Outcome Scale (GOS) PAGEREF _Toc525548324 h 57