Ebook Cardiac arrest - The science and practice of resuscitation medicine (2nd edition): Part 1

(BQ) Part 1 book Cardiac arrest - The science and practice of resuscitation medicine presents the following contents: Introduction, basic science, the pathophysiology of global ischemia and reperfusion, therapy of sudden death. Invite you to consult.

z.f This page intentionally left blank Cardiac Arrest The Science and Practice of Resuscitation Medicine Second edition Cardiac Arrest is the definitive and most comprehensive reference in advanced life support and resuscitation medicine This new edition brings the reader completely up-todate with developments in the field, focusing on practical issues of decision making, clinical management and prevention, as well as providing clear explanations of the science informing the practice The coverage includes information on the latest pharmacotherapeutic options, the latest chest compression techniques and airway management protocols, all backed by clearly explained, evidence-based scientific research The content is consistent with the latest guidelines for practice in this area, as detailed by the major international governing organizations This volume is essential reading for all those working in the hospital environments of emergency medicine, critical care, cardiology and anesthesia, as well as those providing care in the pre-hospital setting, including paramedics and other staff from the emergency services Norman A Paradis is Adjunct Professor of Surgery, University of Colorado Health Sciences Center Henry R Halperin is Professor of Medicine, Radiology, and Biomedical Engineering at the Johns Hopkins University School of Medicine, Baltimore, USA Karl B Kern is Professor of Medicine at the Sarver Heart Center, University of Arizona, USA Volker Wenzel is Associate Professor of Anesthesiology and Critical Care Medicine in the Department of Anesthesiology and Critical Care Medicine of Innsbruck Medical University, Innsbruck, Austria Douglas A Chamberlain CBE is Honorary Professor of Resuscitation Medicine at the School of Medicine, Cardiff University, Wales and Visiting Professor of Cardiology at the University of Brighton, Sussex, UK From reviews of the first edition: It is a tribute to the editors of this book, and the contributors they have selected, that they have managed to produce a book of enormous quality on the science of resuscitation medicine The Lancet The excellent book, the first of its kind in the field of cardiac arrest, provides a balance of theoretical and clinical information It achieves a level of authority and sophistication well beyond that of the advanced cardiac life support guidelines and will be of considerable use to all those practicing or teaching clinical resuscitation The New England Journal of Medicine The book has virtually everything one would ever want to know about the causes of cardiac arrest, the applied physiology, and its treatment Physicians and nurses involved in the management of critically ill or injured patients should have Cardiac Arrest in their personal libraries for ready reference Resuscitation Cardiac Arrest The Science and Practice of Resuscitation Medicine Second edition Editors Norman A Paradis, M.D University of Colorado, Denver, USA Henry R Halperin, M.D., M.A Johns Hopkins University School of Medicine, Baltimore, MD, USA Karl B Kern, M.D University of Arizona, Sarver Heart Center, Tucson, AZ, USA Volker Wenzel, M.D., M.Sc Innsbruck Medical University, Innsbruck, Austria Douglas A Chamberlain CBE, M.D School of Medicine, Cardiff University, Wales, UK Senior Associate Editor Max Harry Weil, M.D Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA Associate Editors Scott M Eleff, M.D William Beaumont Hospital, Royal Oak, MI, USA Terry L Vanden Hoek, M.D University of Chicago, IL, USA Vinay M Nadkarni, M.D Children’s Hospital of Philadelphia, PA, USA Development Editor Pamela Talalay, Ph.D Johns Hopkins University School of Medicine, Baltimore, MD, USA CAMBRIDGE UNIVERSITY PRESS Cambridge, New York, Melbourne, Madrid, Cape Town, Singapore, São Paulo Cambridge University Press The Edinburgh Building, Cambridge CB2 8RU, UK Published in the United States of America by Cambridge University Press, New York www.cambridge.org Information on this title: www.cambridge.org/9780521847001 © Norman A Paradis, Henry R Halperin, Karl B Kern, Volker Wenzel and Douglas A Chamberlain 2007 This publication is in copyright Subject to statutory exception and to the provision of relevant collective licensing agreements, no reproduction of any part may take place without the written permission of Cambridge University Press First published in print format 2007 eBook (EBL) ISBN-13 978-0-511-35489-2 ISBN-10 0-511-35489-4 eBook (EBL) ISBN-13 ISBN-10 hardback 978-0-521-84700-1 hardback 0-521-84700-1 Cambridge University Press has no responsibility for the persistence or accuracy of urls for external or third-party internet websites referred to in this publication, and does not guarantee that any content on such websites is, or will remain, accurate or appropriate Every effort has been made in preparing this publication to provide accurate and up-todate information which is in accord with accepted standards and practice at the time of publication Although case histories are drawn from actual cases, every effort has been made to disguise the identities of the individuals involved Nevertheless, the authors, editors and publishers can make no warranties that the information contained herein is totally free from error, not least because clinical standards are constantly changing through research and regulation The authors, editors and publishers therefore disclaim all liability for direct or consequential damages resulting from the use of material contained in this publication Readers are strongly advised to pay careful attention to information provided by the manufacturer of any drugs or equipment that they plan to use In memory of Harold Paradis, M.D., without whose inspiration this effort would never have been undertaken, and for Christine, without whose patience it would never have been completed N.A.P To my wife, Sharon Tusa Halperin, and children, Victoria and Eric Halperin, whose patience and support inspired me to complete my contributions to this work In memory of Victor Halperin, D.D.S., who inspired me to undertake a career in academic medicine and complete this work H.R.H To Martha, my wife, who always understood that the most worthwhile books are written with friends, and that true friendship develops best while fly fishing, and to Matt, my youngest son, who has helped me keep my perspective that each day is wonderful and full of promise K.B.K To my daughter Katharina, whose love from Innsbruck to the moon and back keeps me going on good days and especially on bad days, and in memory of Gunther and Ute Wenzel And to my friends worldwide providing ideas, critique, encouragement, and hard work V.W To my wife Jennifer, who continues to be incredibly tolerant of a husband who is forever ensconsed in his study and who offers no help with the washing up D.A.C Contents List of contributors Foreword – Myron L Weisfeldt M.D Preface xi xxvii xxxi Part I Introduction A history of cardiopulmonary resuscitation Mickey S Eisenberg, Peter Baskett, and Douglas Chamberlain The epidemiology of sudden death 26 Graham Nichol and David Baker Part II Basic science Global cellular ischemia/reperfusion during cardiac arrest: critical stress responses and the postresuscitation syndrome 51 Kimm Hamann, Dave Beiser, and Terry L Vanden Hoek Genetics, genomics and proteomics in sudden cardiac death 70 Lesley A Kane, Silvia G Priori, Carlo Napolitano, Dan E Arking, and Jennifer E Van Eyk Intracellular signaling during myocardial ischemia 90 Peter H Sugden Electrophysiology of ventricular fibrillation and defibrillation 101 Wei Xiong and Gordon F Tomaselli The neuroendocrine response to global ischemia and reperfusion 128 Martin W Dünser, Stefan Jochberger, Karl-Heinz Stadlbauer, and Volker Wenzel vii viii Contents Inflammatory and Immunologic responses to ischemia and reperfusion 163 Jason S Haukoos, Ronald J Korthuis, and James T Niemann 21 Analysis and predictive value of the ventricular fibrillation waveform 417 Trygve Eftestøl, Hans-Ulrich Strohmenger, and Colin Robertson 22 Etiology, electrophysiology, and myocardial mechanics of pulseless electrical activity Resuscitation research Methodology of laboratory resuscitation research 179 426 Tom P Aufderheide Menekhem Zviman and Henry R Halperin 10 The methodology of clinical resuscitation research 206 Johan Herlitz, Anouk van Alem, Volker Wenzel, and Karl Wegscheider 11 The special problem of consent for resuscitation research Part IV Therapy of sudden death 23 Prevention of sudden cardiac death 449 Catherine Campbell, Ty J Gluckman, Charles Henrikson, Dominique M Ashen, and Roger S Blumenthal 216 Henry R Halperin and Douglas Chamberlain 24 Sequence of therapies during resuscitation: application of CPR 463 Leonard A Cobb Part III The pathophysiology of global ischemia and reperfusion 12 The etiology of sudden death 25 Transthoracic defibrillation 229 Sunil K Sinha, Arthur J Moss, and Hugh G Calkins 13 Global brain ischemia and reperfusion 236 Brian J O’Neil, Robert W Neumar, Uwe Ebmeyer, and Gary S Krause 14 Reperfusion injury in cardiac arrest and cardiopulmonary resuscitation 282 298 326 347 369 550 571 Henry R Halperin and Barry K Rayburn 585 Henry R Halperin 32 Invasive reperfusion techniques 600 Mark G Angelos 389 Uwe Ebmeyer, Laurence M Katz, and Alan D Guerci Tommaso Pellis, Jasmeet Soar, Gavin Perkins, and Raúl J Gazmuri 506 External chest compression: standard and alternative techniques 31 Mechanical devices for cardiopulmonary resuscitation Karl B Kern, James T Niemann, and Stig Steen 20 Pharmacology of cardiac arrest and reperfusion 29 Airway techniques and airway devices 30 Manual cardiopulmonary resuscitation techniques Michael P Frenneaux and Stig Steen 19 Methods to improve cerebral blood flow and neurological outcome after cardiac arrest 28 The physiology of ventilation during cardiac arrest and other low blood flow states Jerry P Nolan and David A Gabbott Perfusion pressures 18 Coronary perfusion pressure during cardiopulmonary resuscitation 496 Ahamed H Idris and Andrea Gabrielli Henry R Halperin 17 Hemodynamics of cardiac arrest 482 Rudolph W Koster, Douglas Chamberlain, and Dianne L Atkins Roger D White, Mick Colquhoun, Carys Sian Davies, Mary Ann Peberdy, and Sergio Timerman Kevin R Ward and Andreas W Prengel 16 Mechanisms of forward flow during external chest compression 26 Automated external defbrillators 27 Public access defibrillation Thomas Aversano 15 Visceral organ ischemia and reperfusion in cardiac arrest 470 Richard E Kerber, Charles D Deakin, and Willis A Tacker, Jr 33 Routes of drug administration Thomas Kerz, Gideon Paret, and Holger Herff 395 614 800 M Baubin, W Rabl and R Hoke caused by equipment failure while 17 were caused by improper handling and neglected safety precautions, respectively; the reason for the remaining episode could not be determined Based on the records of the Emergency Medical Services in King County, where paramedics had treated more than 3000 cardiac arrest patients at that time, the authors estimated the incidence of electrical shocks to ambulance personnel at approximately injury per 1700 shocks In most cases, the physical consequences of such accidental shocks are minor Short-term discomfort and local tingling have been described More serious sequelae included burns and one case of hospital admission for frequent premature ventricular contractions To the best of our knowledge, there are no case reports of death or long-term impairment in personnel after suffering an electric shock during defibrillation or cardioversion of a patient Likewise, we are not aware that such an accidental shock to bystanders has ever resulted in a critical medical condition or even cardiac arrest It is a popular but erroneous belief that a current always travels the path of least resistance Unless there is arcing of electricity from the electrodes, the majority of the total current produced by the defibrillator will travel through the chest The current to which a bystander may be exposed can only be a fraction of the total current, being indirectly proportional to the resistance of the bodies, the bystander’s shoes, the floor and the bed It has yet to be investigated whether such shunt currents are at all capable of reaching the fibrillation threshold and thus inducing VF The safety precautions advocated by the medical authorities and manufacturers to prevent electrical accidents include standard device maintenance procedures, avoidance of excessive amounts of conduction gel during resuscitation (and preferential use of gel pads), giving announcements aloud, checking that everybody stands clear before defibrillator discharge, and ensuring that manual paddles are placed only on either the patient’s chest or in the defibrillator pockets Although the actual risk of being harmed by shunt currents during defibrillation is very low it seems reasonable to follow these rules Danger of fire Defibrillation may set the patient, rescuers, the bed, and medical equipment on fire Severe burns, considerable material damage, and the exigency of ward evacuation have been described repeatedly Such fires are no mysteries of resuscitation; circumstances that may culminate in this hazardous complication are well known and precautions for its prevention are available Three prerequisites must be fulfilled to ignite a fire by defibrillation: (1) an oxygen-enriched atmosphere must exist in the vicinity of the defibrillator electrodes; (2) an electric spark is needed for ignition; and (3) an agent that is combustible must be present If any of these three “ingredients” is absent, a fire is very unlikely An oxygen-enriched atmosphere (OEA) appears to be the basis for ignition Ventilation bags with an oxygen-flow of Ն 10 l/min put next to the patient’s head increase the oxygen concentration of the ambient air at several points around the head and chest of the patient.73 The same finding applies to mechanical ventilator tubes when they are disconnected from the tracheal tube, left close to the patient, and continue to deliver oxygen Also, oxygen masks left on the patient’s face during defibrillation are sufficient to establish an OEA – probably by leakage of oxygen under the edges of the mask.74 Evidence suggests that keeping the ventilation devices m off the patient’s head is safe Clearly, a mechanical ventilator that is left connected to a tracheal tube poses no threat It is a matter of controversy, however, whether a manual ventilation bag that remains connected to a tracheal airway with oxygen leaking from the overflow valve is safe or not Since increased ambient oxygen concentrations have been demonstrated in a corresponding manikin model, it appears prudent to consider this condition as dangerous as well.75 The highest oxygen concentration on the body surface is usually measured in the axilla Indeed, oxygen, being slightly denser than room air, may accumulate in swales and cavities as, for instance, those provided by crumpled sheets or clothing An electric arc or spark is essential to set combustible material on fire by defibrillation Sparks are more likely if resistance of the electrode–skin junction is high This condition occurs when electrode paddles or pads are not in proper contact with the chest across their entire surface, when inadequate conductive gel is used, or when adhesive electrode pads are dried out Case reports have also suggested that too much gel (smeared across the chest) and ECG electrodes next to the defibrillator electrodes may have contributed to fire incidents in the past Oxygen itself is not flammable To feed a fire it needs an agent that is combustible Some agents present during resuscitation are particularly prone to be ignited by a spark in an oxygen-enriched atmosphere These include fine body hair, surface nap fibres found on most fabrics, dust, and others Once one of these easily flammable materials has been ignited, other adjacent matter may catch fire Often, the flame flashes instantaneously over the surface of the bed or patient in a phenomenon referred to as “surfacefibre flame propagation.”76 Spreading of the fire front towards the oxygen source is common, and damage of devices such as the mechanical ventilator have been described Complications of CPR Table 45.2 Safeguards to minimize the risk of fire during defibrillation Prevention of an oxygen-enriched atmosphere Always connect an airway adjunct to oxygen supplies properly Before defibrillation, leave a mechanical ventilator tube properly connected to the tracheal airway, but remove manual ventilation bags and oxygen masks as far away from the patient as practical (at least m) During resuscitation never leave an open oxygen source next to the patient Prevention of sparks Avoid electrode placement over an irregular chest surface If contact gaps, e.g., caused by depressed intercostal spaces, are inevitable, consider anterior-posterior electrode position Do not place paddles or pads over or close to ECG wires or ECG electrodes Shave or, if time permits, clip excessive chest hair under the area of electrode contact (a) Use of manual paddles: Use an appropriate amount of conductive gel Make sure the gel is approved for defibrillation Consider gel-pads as a substitute for jelly Apply firm and even paddle force according to the guidelines Make sure the whole paddle surface is in contact with the skin (b) Use of self-adhesive pads: Check date of expiration and integrity of the pad packaging before application When attaching the pads to the chest wall, make sure that they are not folded, air bubbles are not trapped underneath, and adherence to the skin is complete Remember to change dried-out pads during long-term or repetitive resuscitation according to manufacturer’s advice Removal of flammable material If feasible, move gowns, patient’s clothing, bedding, drapes, curtains, etc from the resuscitation area In conclusion, fires ignited by defibrillation are not rare, but adherence to a few simple rules can prevent this potentially devastating complication (Table 45.2) Danger of explosions In the past, attempted defibrillation through nitroglycerin (glyceryl trinitrate) patches has occasionally resulted in “explosions” including arcing, a loud noise, and smoke This was first interpreted as an actual explosion of the pharmacologic agent In contrast, further investigations concluded that this phenomenon only occurred in medication patches containing metal foil or mesh, and that it appeared to be due to a voltage breakdown resulting from the high resistance of such patches.77–79 This voltagebreakdown follows the same principles as were discussed above in conjunction with burns and may be accompanied by an arc between the defibrillator electrode and the metal foil in the patch As a consequence, perforation of the patch is common Modern transdermal medication patches no longer contain a metal foil Nonetheless, as such patches may increase the resistance at the electrode–skin interface, with the subsequent risk of sparks, burns, and dissipation of defibrillation energy as discussed above, it is reasonable to advise defibrillating personnel not to place defibrillator paddles or pads over any kind of medication patches Patches should be removed Conclusions Most patients who undergo multiple defibrillation attempts will develop at least first-degree burns at the site of electrode attachment Higher cumulative energy will cause more severe burns Repetitive countershocks may be accompanied by a considerable degree of skeletal muscle decomposition, including the risk of rhabdomyolysis At least in adults, clinically relevant postresuscitative impairment of myocardial function so far has not conclusively been shown to be attributable to defibrillation In pacemaker or ICD carriers, medical personnel must be aware that defibrillation can result in temporary or permanent malfunction or breakdown of the device Minor electric shocks may be inflicted to rescue personnel during defibrillation of a patient No case of long-term impairment or lethal outcome of such accidental shocks has been reported in the medical literature, however In contrast, non-therapeutic full capacity transthoracic shocks can be fatal Defibrillation can ignite a fire at the bedside if an oxygen-enriched atmosphere is present; preventive measures are available Safety precautions for defibrillation are discussed above 801 802 M Baubin, W Rabl and R Hoke Complications of artificial respiration Universal complications of artificial respiration Injuries associated with reclination of the cervical spine To keep the airway patent and protected is one of the first steps in resuscitation of collapsed patients The patency of the airway can be maintained by chin lift (performed with one hand at the side of the patient) and jaw thrust (Esmarch maneuver performed with both hands above the patient) and additional head tilt, with or without the assistance of airway device, for example, oropharyngeal or nasopharyngeal airway devices Airway management can be particularly complex when there are facial bone fractures, head injuries, and cervical spine instability.80 Whereas results of some authors indicate that the chin lift technique provides the most consistently adequate airway,81,82 other authors stated that the jaw thrust maneuver is more effective in improving airway patency and ventilation, especially in children.83 During head tilt and the assistance for intubation, the patientЈs neck is put in an extreme reclination and maximal straightening, which leads to a high tension load on the cervical column Typical complications are intimal lesions in the vessels84 and retropharyngeal hemorrhage When the maneuvres are conducted with high force and velocity, the risk is high for injury to the cervical spine itself Elderly people have a higher risk for such osseous lesions, because of degenerative and osteoporotic alterations Spinal cord injury and dislocation of the cervical spine may occur, especially in patients with preexisting trauma Pneumoperitoneum Mechanical ventilation and cardiopulmonary resuscitation can be specific causes of non-surgical pneumoperitoneum Pneumothorax has also been associated with pneumoperitoneum A direct passage through pleural and diaphragmatic defects and a passage via the mediastinum along perivascular connective tissue or major diaphragmatic portals to the retroperitoneum and finally to the peritoneum are considered as mechanisms The management of pneumoperitoneum of suspected thoracic etiology can be conservative when there are no peritoneal signs or a suspicious ruptured viscus.85 Regurgitation and aspiration The risk of gastric regurgitation and subsequent pulmonary aspiration is a recognized complication of cardiac arrest – a risk, that may be further increased by the resuscitative procedure itself A study comparing bag valve mask (BVM) and laryngeal mask airway (LMA) confirmed that when an LMA is used as a first line airway device, regurgitation is relatively uncommon.86 Despite orotracheal intubation, aspiration around the tracheal tube may be a complication provoked by frequent swallowing movements.87 Artificial respiration without devices: gastric distension and rupture Air insufflation in the stomach is a frequent complication of mouth-to-mouth ventilation promoted in the case of airway obstruction The gastric distension interferes with ventilation by elevating the diaphragm, resulting in a decreased lung volume Constant cricoid pressure – the Sellick maneuver – during artificial breathing could prevent gastric distension in these instances and should be recommended.88 Rupture of the stomach is a rare complication of cardiopulmonary resuscitation An incidence of 0.1% has been reported in the literature.69 Between 1970 and 2000 the number of cases referred in the literature did not exceed 30.90 The majority of reported cases have been associated with difficulty in airway management or esophageal intubation (Fig 45.3).91 In an experimental study design, the mean rupture pressure of the human stomach was 73 ϩ / Ϫ 13 mmHg (9.7 ϩ / Ϫ 1.7 kPa) and the mean rupture volume was 2670 ϩ / Ϫ 410 ml A viscoelastic model can be used for representing the relations between pressure and volume as well as pressure and time The site of main ruptures coincides with mesenteric insertion at the lesser gastric curvature The effusion of gastric contents into the lesser omentum and the mediastinum may be responsible for an occasional lack of abdominal symptoms.92 Artificial respiration with devices Tracheal intubation Securing the airway with an endotracheal tube is the gold standard, but excellent success in emergency airway management depends on initial training, retraining, and actual frequency of a given procedure in routine.93 Intubation may result in further injury of oral and/or cervical soft tissue by mechanical damage during the manipulations, especially in a sequence of multiple attempts.94 Undesirable incidents or complications are seen in about 20% of prehospital emergency airway management procedures The most common complications (nϭ201) Complications of CPR are: more than one attempt of intubation (14.4%), vomiting and/or aspiration (6.8%), esophageal intubation (3.2%), and mucosal injuries (1.7%).95 Multiple endotracheal intubation attempts are associated with significant complications, offer limited advantage over bag valve mask, and may possibly affect outcome Indications for field intubations may require review, especially in rural pediatric trauma In the field, more attempts of intubation were necessary compared to planned intubation in operation rooms Airway complications and multiple intubations were associated with transport delay, lower GCS, longer hospital stay, and lower discharge GCS, but were independent of injury severity score, sex, age, and survival.96 In elective intubation, the teeth most likely to be injured are the upper incisors In most cases dental injury is not associated with a pre-event prediction of difficult intubation.97 Compared to metal laryngoscopes plastic blades not fracture any dental model materials; therefore, plastic laryngoscope blades are less likely to cause dental fracture compared with metal blades.98 Chewing on an endotracheal tube may be another cause of tooth damage.99 Such factors must be taken into account in cases of claiming iatrogenic damage Tapia’s syndrome (paralysis of the hypoglossal and recurrent laryngeal nerves) is due to extracranial involvement of the hypoglossal nerve and the recurrent laryngeal branch of the vagal nerve and may be a complication of intubation.100 Use of more than one tube, a narrow laryngeal space, and accidental flexion of the neck contribute to a bilateral recurrent paralysis of the laryngeal nerve.101 Although tracheal rupture is a rare complication of endotracheal intubation,102 if it does occur, the mortality is 75%103 Tracheal rupture leads to pneumothorax and emphysema of subcutaneous tissue and infections Lesions from intubation are always located in the membraneous part and follow the longitudinal axis of the trachea.104 Even the hypopharyngeal tissue can be perforated during intubation.105 Esophageal intubation Cardiac arrest during emergency tracheal intubation is a relatively common problem Airway-related complications play a prominent role in these cases Out of 3035 critically ill patients suffering from cardiopulmonary, traumatic, septic, metabolic, or neurological-based deterioration and requiring emergency airway management, 60 suffered from cardiac arrest Esophageal intubation was a frequent complication (n ϭ 38; 63%), often leading to hypoxemia (97%) and regurgitation (67%) Immediate access to advanced airway devices and endotracheal tube-verifying Fig 45.3 Intestinal insufflation after esophageal intubation devices appears to have a significant impact on the incidence of hypoxemia-driven cardiac arrest.106 Nasotracheal and nasopharyngeal airway Complications such as hemorrhage occur more frequently with the nasotracheal than with the orotracheal route.107 On the other hand, the orotracheal intubation route was significantly associated with a higher frequency of aspiration compared with nasotracheal intubation in children These results suggest that the nasotracheal intubation route is recommended as the first choice for reducing this potential clinical complication.87 Blind nasopharyngeal airway insertion may result in lethal iatrogenic injury when used in a head-injured patient Even an intracranial insertion of a nasopharyngeal airway during resuscitation after trauma has been reported Oropharyngeal airways may be used to assist with ventilation.108 In patients with lesions of the cervical spine, direct laryngoscopy for endotracheal intubation entails the risk of injuring the spinal cord In an attempt to avoid this complication, flexible fiberoptic nasal intubation can be used.109 Alternative airway devices Alternative airway devices have been developed, especially for emergency care systems when the use of endotracheal intubation by prehospital care personnel is restricted by policy or statute, or as a second line airway device These alternative airway devices include Laryngeal Mask Airway (LMA), the Esophageal Obturator Airway (EOA) and Esophageal Gastric Tube Airway (EGTA), the 803 804 M Baubin, W Rabl and R Hoke Pharyngeotracheal Lumen Airway (PTL), and the Esophageal-Tracheal Combitube (ETC) The EGTA adds a Levine tube to the EOA to relieve gastric pressure Ventilation and oxygenation can, in some circumstances, be achieved equally well with the EOA/EGTA device or with endotracheal intubation Alternative airway devices can be inadequate and the complication rate is relatively high The PTL and the ETC seem to provide adequate ventilation and oxygenation with few complications.110 Laboratory and clinical evidence supports the important role of alternative airway devices to mask ventilation and endotracheal intubation in the chain of survival In particular, the laryngeal mask airway (LMA) and ETC proved to be effective alternatives in providing oxygenation and ventilation to the patient in cardiac arrest.111 In a comparative study of patients in cardiopulmonary arrest with ventricular fibrillation, endotracheal tube airway and EGTA were compared Complication rates and success of intubation were similar in the two groups, although only training time was longer for endotracheal intubation.112 The esophageal–tracheal Combitube (ETC) is a ventilatory device consisting of a twin lumen tube with proximal and distal inflatable cuffs The major benefit of the Combitube is that its design and function allow for ventilation through non-laryngoscope-assisted insertion into either the trachea or esophagus.113 Although visualized endotracheal intubation remains the preferred method of airway control, the ETC may be an effective prehospital airway device as both a backup to the endotracheal tube and a primary airway Although the ETC does not require visualization with a laryngoscope, comprehensive training and continuing education are key factors in maintaining skill retention.114 Complications of ETC include subcutaneous emphysema, pneumomediastinum, and pneumoperitoneum In a cadaver study, a protrusion of the anterior wall of the esophagus and distension resulting from inflation of the distal cuff was found, which could lead to esophageal injuries.115,116 In another study118, the serious or potentially lethal complication rate was 3.3 times more common with the use of the EOA/EGTA than with the tracheal tube In a direct comparison of LMA, ETC, and the tracheal tube, the use of the tracheal tube by medical students was difficult and the skills acquired deteriorated significantly over time The LMA, the LT and the ETC seemed to have an advantage over the tracheal tube insofar as the techniques were more easily learned and the skills better retained For the LMA and the ETC, the authors recommended that these alternative devices be included in the medical school curriculum for airway management.118 Insufflation of the stomach with air can be a complication of face mask ventilation in the case of airway obstruction Although the laryngeal mask airway (LMA) has proven of value in airway resuscitation, it has two major failings: a relatively low seal pressure, and lack of access to the alimentary tract These problems led to the development of the LMA-ProSeal, which permits ventilation with higher airway pressures.119 The placement of the ProSeal laryngeal mask airway is said to be significantly easier than for the laryngeal mask airway.120 Cricothyrotomy and tracheotomy Percutaneous transtracheal ventilation has proven useful in emergency airway management Its speed and ease of performance are offset by the need for specialized equipment to accomplish it.121 There is a tendency toward carbon dioxide retention and poor alveolar washout The most common complication is subcutaneous emphysema caused by incorrect placement of the catheter.122 Infections are a rare complication of percutaneous transtracheal ventilation In a reported case, the contamination of the deep neck spaces facilitated by pressure dissection of the fascial planes led to cervical osteomyelitis.123 Tracheotomy and coniotomy are procedures that cause frequent early and later complications; therefore, there must be a rigorous indication that they are necessary If emergency airway access is needed and translaryngeal intubation is not possible, a cricothyroidotomy should be considered.124 Careful management and expert nursing support can prevent many later complications “Minimally invasive” cricothyroidotomy devices are now available for the professional health care provider who is not proficient or comfortable with performing an emergency surgical tracheotomy or cricothyroidotomy.111 The main indication for cricothyroidotomy is the inability to establish an airway by intubation, usually in a situation of possible neck injury or severe facial trauma The use of emergency cricothyroidotomy is supported in situations in which intubation is not successful or thought not to be safe Tracheostomy subsequent to emergency cricothyroidotomy does not necessarily reduce airwayrelated morbidity in these patients.125 Conclusions Ventilation with the objective of oxygenating the blood is a decisive step in resuscitation For this purpose the airway must be kept patent and protected First, the indication for Complications of CPR artificial airway management must be examined carefully Depending on preexisting conditions like head and cervical spine injuries, airway management can be particularly complex Any action taken – even mouth-to-mouth resuscitation – is subject to more or fewer complications, some of them lifethreatening The rescuer should be aware of these hazards and minimize their frequency by continuing education and comprehensive training Concomitantly, refraining from indicated airway management and artificial ventilation leads to a lethal outcome in every patient New advanced airway devices can be helpful and are increasingly included in the medical staff training for airway management Professional skills have to be achieved and sustained: practice makes perfect REFERENCES 2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Core Science with Treatment Recommendations Resuscitation 2000; 67: 203–204 Katz, A., Henkin, J & Ovsyshcher, I.A Transient complete atrioventricular block induced by a chest thump in a patient with ventricular tachycardia Int J Cardiol 1989; 23: 395–396 Sclarovsky, S., Kracoff, O., Arditi, A & et al Ventricular tachycardia “pleomorphism” induced by chest thump Chest 1982; 81: 97–99 Cotoi, S Precordial thump and termination of cardiac re-entrant tachyarrythmias Am Heart J 1981; 101: 675–677 Penneington, J.E., Taylor, J & Lown, B Chest thump for reverting ventricular tachycardia N Engl J Med 1970; 26: 1192–1195 Hoke, R.S & Chamberlain, D Skeletal chest injuries secondary to cardiopulmonary resuscitation Resuscitation 2004; 63: 327–338 Black, C.J., Busuttil, A & Robertson, C Chest wall injuries following cardiopulmonary resuscitation Resuscitation 2004; 63: 339–343 Himmelhoch, S.R., Dekker, A., Gazzaniga, A.B & Like, A.A Closed-chest cardiac resuscitation A prospective clinical and pathological study N Engl J Med 1964; 270: 118–122 Baubin, M., Sumann, G., Rabl, W., Eibl, G., Wenzel, V & Mair, P Increased frequency of thorax injuries with ACD-CPR Resuscitation 1999; 41: 33–38 10 Krischer, J.P., Fine, E.G., Davis, J.H & Nagel, E.L Complications of cardiac resuscitation Chest 1987; 92: 287–291 11 Saternus, K.S Direkte und indirekte Traumatisierung bei der Reanimation Z Rechtsmed 1981; 86: 161–174 12 Kloss, T., Puschel, K., Wischhusen, F., Welk, I., Roewer, N & Jungck, E Reanimationsverletzungen Anaesth Intensivther Notfallmed 1983; 18: 199–203 13 Brown, J., Rogers, J & Soar, J Cardiac arrest during surgery and ventilation in the prone position: a case report and a systematic review Resuscitation 2001; 50: 233–238 14 Jackson, C.T & Greendyke, R.M Pulmonary and cerebral fat embolism after closed-chest cardiac massage Surg Gynec Obstet 1965; 120: 25–27 15 Yarnoff, M Incidence of bone marrow embolism due to closed-chest cardiac massage N Engl J Med 1963; 269: 837 16 Patterson, R.H., Burns, W.A & Jannotta, F.S Complications of external cardiac resuscitation: a retrospective review and survey of the literature Med Ann Distr Columb 1974; 43: 389–393 17 Bynum, W.R., Connell, R.M & Hawk, W.A Causes of death after external cardiac massage: analysis of observations on fifty consecutive autopsies Cleve Clin Q 1963; 30: 147–151 18 Baringer, J.R., Salzman, E.W., Jones, W.A & Friedlich, A.L External cardiac massage N Engl J Med 1961; 265: 62–65 19 Powner, D.J., Holcombe, P.A & Mello, L.A Cardiopulmonary resuscitation-related injuries Crit Care Med 1984; 12: 54–55 20 Winkel, E.C & Brown, W.G Bone marrow embolism following closed chest cardiac message J Am Med Assoc 1961; 178: 329–331 21 Lurie, K.G., Shultz, J.J., Callaham, M.L et al Evaluation of active compression–decompression CPR in victims of out-ofhospital cardiac arrest J Am Med Assoc 1994; 271: 1405–1411 22 Mauer, D., Schneider, T., Dick, W., Withelm, A., Elich, D & Mauer, M Active compression-decompression resuscitation: a prospective, randomized study in a two-tiered EMS system with physicians in the field Resuscitation 1996; 33: 125–134 23 Cohen, T.J., Goldner, B.G., Maccaro, B.C., et al A comparison of active compression–decompression cardiopulmonary resuscitation with standard cardiopulmonary resuscitation for cardiac arrests occurring in the hospital N Engl J Med 1993; 329: 1918–1921 24 Plaisance, P., Adnet, F., Vicaut, E et al Benefit of active compression–decompression cardiopulmonary resuscitation as a prehospital advanced cardiac life support A randomized multicenter study Circulation 1997; 95: 955–961 25 Luiz, T., Ellinger, K & Denz, C Active compression–decompression cardiopulmonary resuscitation does not improve survival in patients with prehospital cardiac arrest in a physician-manned emergency medical system J Cardiothorac Vasc Anesth 1996; 10: 178–186 26 Rabl, W., Baubin, M., Broinger, G & Scheithauer, R Serious complications from active compression–decompression cardiopulmonary resuscitation Int J Legal Med 1996; 109: 84–89 27 Rabl, W., Baubin, M., Haid, C., Pfeiffer, K.P & Scheithauer, R Review of active compression–decompression cardiopulmonary resuscitation (ACD-CPR) Analysis of iatrogenic complications and their biomechanical explanation Forens Sci Int 1997; 89: 175–183 28 Lafuente-Lafuente, C & Melero-Bascones, M Active chest compression–decompression for cardiopulmonary resuscitation Cochrane Database Syst Rev 2002;(3):CD002751 805 806 M Baubin, W Rabl and R Hoke 29 Mauer, D.K., Nolan, J., Plaisance, P et al Effect of active compression–decompression resuscitation (ACD-CPR) on survival: a combined analysis using individual patient data Resuscitation 1999; 41: 249–256 30 Steen, S., Liao, Q., Pierre, L., Paskevicius, A & Sjöberg, T Evaluation of LUCAS, a new device for automatic mechanical compression and active decompression resuscitation Resuscitation 2002; 55: 285–299 31 Steen, S., Sjöberg, T., Olsson, P & Young, M Treatment of outof-hospital cardiac arrest with LUCAS, a new device for automatic mechanical compression and active decompression resuscitation Resuscitation 67; 2005: 25–30 32 Timerman, S., Luis Francisco Cardoso, L.F., Ramires, J.A & Halperin, H Improved hemodynamic performance with a novel chest compression device during treatment of in-hospital cardiac arrest Resuscitation 2004; 61: 273–280 33 Hart, A.P., Azar, V.J., Hart, K.R & Stephens, B.G Autopsy artifact created by the Revivant AutoPulse resuscitation device J Forens Sci 2005; 50: 1–5 34 Buckman, R.F Jr., Badellino, M.M., Eynon, C.A et al Openchest cardiac massage without major thoracotomy: metabolic indicators of coronary and cerebral perfusion Resuscitation 1997; 34: 247–253 35 Rozenberg, A., Incagnoli, P., Delpech, P et al Prehospital use of minimally invasive direct cardiac massage (MID-CM): a pilot study Resuscitation 2001; 50: 257–262 36 Moore, E.E., Mattox Kl & Feliciano, D.V Trauma 2nd edn New York: McGraw-Hill, 1991: 181–193 37 Schwab, T.M., Callaham, M.L., Madsen, C.D & Utecht, T.A A randomized clinical trial of active compression–decompression CPR vs standard CPR in out-of-hospital cardiac arrest in two cities J Am Med Assoc 1995; 273: 1261–1268 38 Lederer, W., Mair, D., Rabl, W & Baubin, M Frequency of rib and sternum fractures associated with out-of-hospital cardiopulmonary resuscitation is underestimated by conventional chest X-ray Resuscitation 2004; 60: 157–162 39 Baubin, M., Rabl, W., Pfeiffer, K.P., Benzer, A & Gilly, H Chest injuries after active compression–decompression cardiopulmonary resuscitation in cadavers Resuscitation 1999; 43: 9–15 40 Spevak, M.R Cardiopulmonary resuscitation and rib fractures in infants A post-mortem radiologic-pathologic study J Am Med Assoc 1994; 272: 617–618 41 Feldman, K.W & Brewer, D.K Child abuse, cardiopulmonary resuscitation, and rib fractures Pediatrics 1984; 73: 339–342 42 Bush, C.M., Jones, J.S., Cohle, S.D & Johnson, H Pediatric injuries from cardiopulmonary resuscitation Ann Emerg Med 1996; 28: 40–44 43 Price, E.A., Rush, L.R., Perper, J.A & Bell, M.D Cardiopulmonary resuscitation-related injuries and homicidal blunt abdominal trauma in children Am J Forens Med Pathol 2000; 21: 307–310 44 Betz, P & Liebhardt, E Rib fractures in children – resuscitation or child abuse? Int J Leg Med 1994; 106: 215–218 45 Paaske, F., Hart Hansen, J.P., Koudahl, G & Olsen, J 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 Complications of closed-chest cardiac massage in a forensic autopsy material Dan Med Bull 1968; 15: 225–230 Bjork, R.J., Snyder, B.D., Campion, B.C & Loewenson, R.B Medical complications of cardiopulmonary arrest Arch Intern Med 1982; 142: 500–503 Meyer, P.F., Gadsby, P.D., Van Sickle, D., Schoenlein, W.E., Foster, K.S & Graber, G.P Impedance-gradient electrode reduces skin irritation induced by transthoracic defibrillation Med Biol Eng Comput 2005; 43: 225–229 Pagan-Carlo, L.A., Stone, M.S & Kerber, R.E Nature and determinants of skin “burns” after transthoracic cardioversion Am J Cardiol 1997 79: 689–691 Ambler, J.J., Zideman, D.A & Deakin, C.D The effect of topical non-steroidal anti-inflammatory cream on the incidence and severity of cutaneous burns following external DC cardioversion Resuscitation 2005; 65: 173–178 Deakin, C.D., Sado, D.M., Petley, G.W & Clewlow, F Differential contribution of skin impedance and thoracic volume to transthoracic impedance during external defibrillation Resuscitation 2004; 60: 171–174 Deakin, C.D., Sado, D.M., Petley, G.W & Clewlow, F Determining the optimal paddle force for external defibrillation Am J Cardiol 2002 90: 812–813 Bissing, J.W & Kerber, R.E Effect of shaving the chest of hirsute subjects on transthoracic impedance to self-adhesive defibrillation electrode pads Am J Cardiol 2000 86: 587–589 Sado, D.M., Deakin, C.D., Petley, G.W & Clewlow, F Comparison of the effects of removal of chest hair with not doing so before external defibrillation on transthoracic impedance Am J Cardiol 2004 93: 98–100 Corbitt J.D Jr., Sybers, J & Levin, J.M Muscle changes of the anterior chest wall secondary to electrical countershock Am J Clin Pathol 1969; 51: 107–112 Vogel, U., Wanner, T & Bultmann, B Extensive pectoral muscle necrosis afterdefibrillation: nonthermal skeletal muscle damage caused by electroporation Intensive Care Med 1998; 24: 743–745 Grubb, N.R., Fox, K.A & Cawood, P Resuscitation from outof-hospital cardiac arrest: implications for cardiac enzyme estimation Resuscitation 1996; 33: 35–41 Mullner, M., Sterz, F., Binder, M et al Creatine kinase and creatine kinase-MB release after nontraumatic cardiac arrest Am J Cardiol 1996 77: 581–585 Mattana, J & Singhal, P.C Determinants of elevated creatine kinase activity and creatine kinase MB-fraction following cardiopulmonary resuscitation Chest 1992; 101: 1386–1392 Babbs, C.F., Tacker, W.A., VanVleet, J.F., Bourland, J.D & Geddes, L.A Therapeutic indices for transchest defibrillator shocks: effective, damaging, and lethal electrical doses Am Heart J 1980; 99: 734–738 Yabe, S., Smith, W.M., Daubert, J.P., Wolf, P.D., Rollins, D.L & Ideker, R.E Conduction disturbances caused by high current density electric fields Circ Res 1990; 66: 1190–1203 Niemann, J.T., Walker, R.G & Rosborough, J.P Intracardiac Complications of CPR 62 63 64 65 66 67 68 69 70 71 72 73 74 75 76 77 78 voltage gradients during transthoracic defibrillation: implications for postshock myocardial injury Acad Emerg Med 2005; 12: 99–105 Walker, R.G., Melnick, S.B., Chapman, F.W., Walcott, G.P., Schmitt, P.W & Ideker, R.E Comparison of six clinically used external defibrillators in swine Resuscitation 2003; 57: 73–83 Jones, J.L., Lepeschkin, E., Jones, R.E & Rush, S Response of cultured myocardial cells to countershock-type electric field stimulation Am J Physiol 1978; 235: H214–H222 Morrow, D.A & Antman, E.M Cardiac marker elevation after cardioversion: sorting out chicken and egg Eur Heart J 2000; 21: 171–173 Berg, R.A., Chapman, F.W., Berg, M.D., et al Attenuated adult biphasic shocks compared with weight-based monophasic shocks in a swine model of prolonged pediatric ventricular fibrillation Resuscitation 2004; 61: 189–197 Berg, R.A., Samson, R.A., Berg, M.D et al Better outcome after pediatric defibrillation dosage than adult dosage in a swine model of pediatric ventricular fibrillation J Am Coll Cardiol 2005 45: 786–789 Niemann, J.T., Burian, D., Garner, D & Lewis, R.J Monophasic versus biphasic transthoracic countershock after prolonged ventricular fibrillation in a swine model J Am Coll Cardiol 2000; 36: 932–938 Xie, J., Weil, M.H., Sun, S et al High-energy defibrillation increases the severity of postresuscitation myocardial dysfunction Circulation 1997; 96: 683–688 Altamura, G., Bianconi, L., Lo Bianco, F et al Transthoracic DC shock may represent a serious hazard in pacemaker dependent patients Pacing Clin Electrophysiol 1995; 18: 194–198 Bullock, I & Colquhoun, M Advanced Life Support Instructor Manual Resuscitation Council UK, London, 2001 Montauk, L Lethal defibrillator mishap Ann Emerg Med 1997; 29: 825 Gibbs, W., Eisenberg, M & Damon, S.K Dangers of defibrillation: injuries to emergency personnel during patient resuscitation Am J Emerg Med 1990; 8: 101–104 Robertshaw, H & McAnulty, G Ambient oxygen concentrations during simulated cardiopulmonary resuscitation Anaesthesia 1998; 53: 634–637 Miller, P.H Potential fire hazard in defibrillation J Am Med Assoc 1972; 221: 192 Cantello, E., Davy, T.E & Koenig, K.L The question of removing a ventilation bag before defibrillation J Accid Emerg Med 1998; 15:286 Bruley, M & Lavanchy, C Oxygen-enriched fires during surgery of the head and neck In Stoltzfus, J., Benz, F & Stradling, J (eds.) Flammability and Sensitivity of Materials in Oxygen-Enriched Atmospheres Vol ASTM STP 1040 Philadelphia, PA: American Society for Testing and Materials, 1989: 392–405 Babka, J.C Does nitroglycerin explode? N Engl J Med 1983; 309: 379 Kuhnen, R., Nitsch, J & Luderitz, B Explosion von 79 80 81 82 83 84 85 86 87 88 89 90 91 92 93 94 Nitropflastern bei Defibrillation Deutsche Medizinische Wochenschrift 1985; 110: 37 Liddle, R & Richmond, W Investigation into voltage breakdown in glyceryl trinitrate patches Resuscitation 1998; 37: 145–148 Lim, B.L Airway management – when and how? Singapore Med J 2001; Suppl 1: 43–45 Guildner, C.W Resuscitation – opening the airway A comparative study of techniques for opening an airway obstructed by the tongue JACEP 1976; 5: 588–590 Roth, B., Magnusson, J., Johansson, I., Holmberg, S & Westrin, P Jaw lift – a simple and effective method to open the airway in children Resuscitation 1998; 39: 171–174 Bruppacher, H., Reber, A., Keller, J.P., Geiduschek, J., Erb, T.O & Frei, F.J The effects of common airway maneuvers on airway pressure and flow in children undergoing adenoidectomies Anesth Analg 2003; 97: 29–34 Saternus, K.S & Fuchs, V Verletzungen der A carotis communis durch Reanimationsmaflnahmen Z Rechtsmed 1982; 88: 305–311 Mularski, R.A., Sippel, J.M & Osborne, M.L Pneumoperitoneum: a review of nonsurgical causes Crit Care Med 2000; 28: 2638–2644 Stone, B.J., Chantler, P.J & Baskett, P.J The incidence of regurgitation during cardiopulmonary resuscitation: a comparison between the bag valve mask and laryngeal mask airway Resuscitation 1998; 38: 3–6 Amantea, S.L., Piva, J.P., Sanches, P.R & Palombini, B.C Oropharyngeal aspiration in pediatric patients with endotracheal intubation Pediatr Crit Care Med 2004; 5: 152–156 Ghirga, G., Ghirga, P., Palazzi, C., Pipere, M & Colaiacomo, M Bag-mask ventilation as a temporizing measure in acute infectious upper-airway obstruction: does it really work? Pediatr Emerg Care 2001; 17: 444–446 Reiger, J., Eritscher, C., Laubreiter, K., Trattnig, J., Sterz, F., Grimm, G Gastric rupture – an uncommon complication after successful cardiopulmonary resuscitation: report of two cases Resuscitation 1997; 35: 175–178 Piardi, T., D’Adda, F., Palmieri, F., Vettoretto, N., Lanzi, S & Pouche, A Shock and dyspnea after cardiopulmonary resuscitation: a case of iatrogenic gastric rupture Chir Ital 2000; 52: 593–596 Offerman, S.R., Holmes, J.F & Wisner, D.H Gastric rupture and massive pneumoperitoneum after bystander cardiopulmonary resuscitation J Emerg Med 2001; 21: 137–139 Rabl, W., Ennemoser, O., Tributsch, W & Ambach, E Iatrogenic ruptures of the stomach after balloon tamponade Two case reports: viscoelastic model Am J Forens Med Pathol 1995; 16: 135–139 Von Goedecke, A., Keller, C., Voelckel, W.G., et al Mask ventilatation as an exit strategy of endotracheal intubation Anaethesist 2005; in press Darok, M Injuries resulting from resuscitation procedures In Tsokos, M (Ed.) Forensic Pathology Reviews Vol Humana Press Inc.; Totowa,NJ Chapter 13: 293–303 807 808 M Baubin, W Rabl and R Hoke 95 Thierbach, A., Piepho, T., Wolcke, B., Küster, S & Dick, W Präklinische Sicherung der Atemwege Erfolgsraten und Komplikationen Anaesthesist 2004; 53: 543–550 96 Ehrlich, P.F., Seidman, P.S., Atallah, O., Haque, A & Helmkamp, J Endotracheal intubations in rural pediatric trauma patients J Pediatr Surg 2004; 39: 1376–1380 97 Givol, N., Gershtansky, Y., Halamish-Shani, T., Taicher, S., Perel, A & Segal, E Perianesthetic dental injuries: analysis of incident reports J Clin Anesth 2004; 16: 173–176 98 Itoman, E.M., Kajioka, E.H & Yamamoto, L.G Dental fracture risk of metal vs plastic laryngoscope blades in dental models Am J Emerg Med 2005; 23: 186–189 99 Quinn, J.B., Schultheis, L.W & Schumacher, G.E A tooth broken after laryngoscopy: unlikely to be caused by the force applied by the anesthesiologist Anesth Analg 2005; 100: 594–596 100 Cinar, S.O., Seven, H., Cinar, U & Turgut, S Isolated bilateral paralysis of the hypoglossal and recurrent laryngeal nerves (Bilateral Tapia’s syndrome) after transoral intubation for general anesthesia Acta Anaesthesiol Scand 2005; 49: 98–99 101 Hattori, S., Ohata, H & Dohi, S [Bilateral recurrent laryngeal nerve paralysis in a child following a neurosurgical operation] [Article in Japanese] Masui 2005; 54: 683–686 102 Schonfelder, K., Thieme, V & Olthoff, D Iatrogenic injuries of the trachea Anaesthesiol Reanim 2004; 29: 8–11 103 Doherty, K.M., Tabaee, A., Castillo, M & Cherukupally, S.R Neonatal tracheal rupture complicating endotracheal intubation: a case report and indications for conservative management Int J Pediatr Otorhinolaryngol 2005; 69: 111–116 104 Kaloud, H., Smolle-Juettner, F.M., Prause, G & List, W.F Iatrogenic ruptures of the tracheobronchial tree Chest 997; 112: 774–778 105 Koscielny, S & Gottschall, R Perforation of the hypopharynx as a rare life-threatening complication of endotracheal intubation Anaesthesist 2005 in press 106 Mort, T.C The incidence and risk factors for cardiac arrest during emergency tracheal intubation: a justification for incorporating the ASA Guidelines in the remote location J Clin Anesth 2004; 16: 508–516 107 Piepho, T., Thierbach, A & Werner, C Nasotracheal intubation: look before you leap Br J Anaesth 2005; 94: 859–860 108 Martin, J.E., Mehta, R., Aarabi, B., Ecklund, J.E., Martin, A.H & Ling, G.S Intracranial insertion of a nasopharyngeal airway in a patient with craniofacial trauma Mil Med 2004; 169: 496–497 109 Fuchs, G., Schwarz, G., Baumgartner, A., Kaltenbock, F., VoitAugustin, H & Planinz, W Fiberoptic intubation in 327 neurosurgical patients with lesions of the cervical spine J Neurosurg Anesthesiol 1999; 11: 11–16 110 Pepe, P.E., Zachariah, B.S & Chandra, N.C Invasive airway techniques in resuscitation Ann Emerg Med 1993; 22: 393–403 111 Gabrielli, A., Layon, A.J., Wenzel, V., Dorges, V & Idris, A.H Alternative ventilation strategies in cardiopulmonary resuscitation Curr Opin Crit Care 2002; 8: 199–211 112 Shea, S.R., MacDonald, J.R & Gruzinski, G Prehospital endotracheal tube airway or esophageal gastric tube airway: a critical comparison Ann Emerg Med 1985; 14: 102–112 113 Stoppacher, R., Teggatz, J.R & Jentzen, J.M Esophageal and pharyngeal injuries associated with the use of the esophageal-tracheal Combitube J Forens Sci 2004; 49: 586–591 114 Atherton, G.L & Johnson, J.C Ability of paramedics to use the Combitube in prehospital cardiac arrest Ann Emerg Med 1993; 22: 1263–1268 115 Vezina, D., Lessard, M.R., Bussieres, J., Topping, C & Trepanier, C.A Complications associated with the use of the esophageal–tracheal combitube Can J Anaesth 1998; 45: 76–80 116 Vezina, D., Trepanier, C.A., Lessard, M.R & Bussieres, J Esophageal and tracheal distortion by the esophageal–tracheal combitube: a cadaver study Can J Anaesth 1999; 46: 393–397 117 Hankins, D.G., Carruthers, N., Frascone, R.J., Long, L.A & Campion, B.C Complication rates for the esophageal obturator airway and endotracheal tube in the prehospital setting Prehosp Disaster Med 1993; 8: 117–121 118 Tiah, L., Wong, E., Chen, M.F & Sadarangani, S.P Should there be a change in the teaching of airway management in the medical school curriculum? Resuscitation 2005; 64: 87–91 119 Rosenblatt, W.H The use of the LMA-ProSeal in airway resuscitation Anesth Analg 2003; 97: 1773–1775 120 Asai, T., Murao, K & Shingu, K Efficacy of the ProSeal laryngeal mask airway during manual in-line stabilisation of the neck Anaesthesia 2002; 57: 918–920 121 Jorden, R.C Percutaneous transtracheal ventilation Emerg Med Clin North Am 1988; 6: 745–752 122 Dunlap, L.B & Oregon, E A modified, simple device for the emergency administration of percutaneous transtracheal ventilation JACEP 1978; 7: 42–46 123 Newlands, S.D & Makielski, K.H Cervical osteomyelitis after percutaneous transtracheal ventilation and tracheotomy Head Neck 1996; 18: 295–8 124 Heffner, J.E The technique of tracheotomy and cricothyroidotomy When to operate and how to manage complications J Crit Illn 1995; 10: 561–568 125 DeLaurier, G.A., Hawkins, M.L., Treat, R.C & Mansberger, A.R Jr Acute airway management Role of cricothyroidotomy Am Surg 1990; 56: 12–15 46 Bringing it all together: state-of-the-art therapy for cardiac arrest Max Harry Weil and Wanchun Tang Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA Introduction The history of CPR is in part documented in the Old Testament,1 but the science of CPR is but a half century old and is still emerging from its infancy.2 Accordingly, it is not unexpected and certainly not shameful that as the science of resuscitation goes forward, we must sometimes retreat as often as we advance Yet, that is indeed progress and inevitably the path that is characteristic of meaningful achievements in science and medicine Airway techniques and devices One size does not fit all3 The vast majority of sudden deaths in children and, indeed, in victims under the age of 40 years are attributable to failure of ventilation Accordingly, either mechanical obstruction by foreign body, laryngospasm, or laryngeal edema, or bronchoconstriction, constrains air exchange Neuromuscular or skeletal injury, including intrathoracic crises such as pneumothorax, may account for death, though typically not sudden death It is in these settings that the priority is establishment and maintenance of a patent airway and external ventilation Since a majority of the foreign bodies that are swallowed by children and adults lodge in the posterior pharynx, the rescuer is the person best prepared to remove these promptly Hence, the traditional (A) of the ABC survives, especially for children and young adults and in settings of witnessed cardiac arrest when respiratory distress with paradoxical chest and abdominal movements and especially stridor precedes loss of consciousness There has been an appropriate re-examination of the role of routine endotracheal intubation during CPR, whether in the field or in the hospital For practical purposes, endotracheal intubation interrupts chest compression The predominance of evidence now favors clearance of the airway, but coincident with starting chest compression Even among professional rescuers, there is an unduly high incidence of initially failed intubation and potentially fatal esophageal intubation There is trauma to the airway with bleeding after emergency intubations out-of-hospital in as many as 30% of attempted intubations Routine endotracheal intubation during CPR is therefore now disadvised The alternative is that of a more reliable and less traumatic method of airway control, namely the use of a laryngeal mask airway (LMA) The LMA may be inserted rapidly and securely by a minimally trained professional rescuer with initial benefits comparable to those of endotracheal tubes.4 Drug administration The routine of establishing a route by which resuscitative drugs may be delivered into the central circulation was prompted, in part, by the priority and essentially universal use of epinephrine, atropine, sodium bicarbonate, calcium gluconate or chloride, and lidocaine beginning in the 1960s Intracardiac injection lost favor because it had questionable effectiveness and a risk of serious injury Endotracheal administration survived as an alternative Yet none of these drugs nor any routine pharmaceutical intervention can now be regarded as of proven benefit, even treatment with epinephrine This is more directly Cardiac Arrest: The Science and Practice of Resuscitation Medicine 2nd edn., ed Norman Paradis, Henry Halperin, Karl Kern, Volker Wenzel, Douglas Chamberlain Published by Cambridge University Press © Cambridge University Press, 2007 809 810 M.H Weil and W Tang addressed below Accordingly, the assumption that there is a high priority for establishment of a route for drug administration routinely during CPR is now not sustained Nevertheless, there are major exceptions Intravenous access is required for volume repletion after volume depletion and especially exsanguinations, for administration of specific antidotes to drug intoxication, and for emergency management of major electrolyte or endocrine abnormalities, especially hyperkalemia Ready access to the central circulation may be gained through the internal jugular or subclavian veins Although the supraclavicular approach to the jugular or the subclavian vein has been utilized during CPR, this is inevitably a challenging procedure during chest compression Femoral vein cannulation may be accomplished without interruption of CPR, but the site is less predictable Evidence favoring endobronchial administration of drugs is quite controversial As stated above, the evidence favoring its use is not persuasive Absorption is erratic and drugs accumulate such that effects are of unpredictable onset and duration This route would best be viewed as a last resort in instances in which venous access for specific indications becomes a priority A new development has been intraosseous access to the central circulation Employed initially with high success, in children, the technique has been expanded for use in adults Commercial kits are now available Ease of insertion by trained operators, usually into the tibia, and confirmation of appropriate placement provides a highly effective option for reliable and minimally invasive access to the central circulation.5 Ventilation Methods by which pulmonary gas exchange is restored by artificial ventilation represent the very foundation of resuscitation medicine Yet objective evidence of its lifesaving value during routine CPR after sudden death has greatly diminished Most important, delays in instituting or maintaining chest compression for external ventilation have been shown to have adverse effects on outcomes There is persuasive physiological rationale and experimental confirmation that in settings of cardiac arrest due to sudden death and therefore in the absence of asphyxia, chest compressions without ventilation not compromise outcomes To the contrary, positive pressure breathing, whether by mouth-to-mouth, mouth-to-nose, valved bag and mask, or mechanical ventilators increases intrathoracic pressure and thereby impedes cardiac filling in close relationship to the tidal volumes and the rates at which breaths are delivered Accordingly, the greater the tidal volumes and the higher the frequency, the less is the cardiac output generated by chest compression Hyperventilation resulting in extremes of hypocapnia also may compromise the success of resuscitation.6 There is some optimism that these adversities may be mitigated by use of the impedance threshold valve Greatly reduced pulmonary blood flow requires greatly reduced minute volumes for adequate alveolar ventilation Hence, as little as 300 mL of tidal volume may be adequate for the average adult patient when cardiac output is likely to be less than 20% of normal during CPR Whether hyperventilationinduced hypocapnia and specifically the marked reduction in arterial PCO2 is itself detrimental has not as yet been secured The demotion of ventilations as a priority intervention, however, does not apply to asphyxial cardiac arrest due to drowning or airway obstruction or to pediatric and neonatal resuscitation Whereas there is no secure proof that increasing the inspired oxygen concentrations delivered into or near the airway improves outcomes, there is sufficient rationale and no adverse effects have been identified Public access defibrillation The enthusiasm for early use of automated external defibrillators (AEDs) was understandably ignited by remarkably successful experiences in Rochester, Minnesota, especially by police first responders; in the Las Vegas casinos; in the Chicago airports, in part by untrained rescuers; and by Basic Life Support/AED trained cabin attendants in flight.7 The ultimate life-saving benefits have been less impressive, however, for at least three reasons First, there is persuasive evidence of benefit in public settings, but the preponderance of cardiac arrests occur in the home Second, there is a remarkable decrease in the incidence of sudden death presenting as ventricular fibrillation (VF) both in- and out-of-hospital The overall incidence has decreased below 50% Third, it is now apparent that the non-professional rescuer’s initial resuscitation effort may have been distracted by prioritizing defibrillation therefore engendering delays in initiating and maintaining uninterrupted chest compression Accordingly, chest compression has once again become the primary and initial intervention for both lay and professional rescuers during out-of-hospital CPR, except perhaps for witnessed sudden death during the initial to minutes and asphyxial cardiac arrest Bringing it all together Sequencing CPR There is much merit in the proposal by Weisfeldt and Becker8 to identify three time-sensitive phases of resuscitation after cardiac arrest Nonetheless, these apply primarily to sudden death of cardiac cause, in contrast to either cardiac arrest in settings of asphyxia or exsanguination The first is the electrical phase which the authors estimate to be minutes It is the phase during which electrical conversion takes precedence The second phase extends from to 10 minutes and this is the time window for restoring blood flow that currently is performed almost entirely with precordial compression or, in uncommon instances of chest surgery or trauma to the thorax, open chest direct cardiac compression The third and final phase is the metabolic phase in which there is myocardial (and cerebral) ischemic injury with progression to cell death The heart itself loses compliance and there is evidence of progression to a stone heart As highlighted by Cobb,9 chest compression with effort to restore circulation promptly continues to take the lead as the initial intervention in all instances of sudden death, except for opening of the airway and restoring breathing in settings of asphyxial cardiac arrest, in addition to precordial compression Prevention Sudden cardiac death is epidemic, and the predominant cause of cardiac arrest in industrialized nations is cardiovascular disease, specifically atherosclerosis A remarkable 70% of all deaths in the United States are now attributed to coronary or cerebral vascular diseases which terminate in myocardial infarction or stroke Prevention of sudden death therefore appropriately focuses on prevention of identifiable risk factors Though family history may in part account for as many as 50% of fatal atherosclerotic vascular events, evidence favors lifestyle interventions and, when that alone is of limited effectiveness, appropriate pharmacological interventions It is likely that understanding of a “metabolic syndrome”10 has been both a conceptual and a pragmatic advance The hallmarks include a combination of abdominal obesity, hypertension, hypertriglyceridemia, fasting hyperglycemia, and a disproportionately higher LDL cholesterol and a lower HDL cholesterol Lifestyle interventions include diet, exercise, and cessation of smoking Pharmacological interventions include control of hypertension, hyperglycemia, and hyperlipidemia and, in some instances, the administration of antiplatelet agents Relatively rare causes of sudden death, especially in children and younger adults, are genetic causes of heart disease These are now better identified by genotyping11 and include hypertrophic (subaortic, septal) cardiomyopathies, long QT syndromes, Brugada syndrome, socalled catecholaminogenic polymorphic ventricular tachycardia and arrhythmogenic right ventricular dysplasia Syncope is an important warning sign Perhaps the largest cause of cardiac death is that of endstage heart failure when ejection fractions decline to less than 30% Both survivors of cardiac arrest and individuals who are identifiably at high risk of sudden death are candidates for internally implanted defibrillators and this has proven to be a major advance for prolonging survival in such patients Vasopressor agents and sodium bicarbonate Perhaps no two subjects bearing on CPR have been debated more vigorously and, from our vantage point, with greater emotional fervor than the use of vasopressor agents and sodium bicarbonate Epinephrine has been the singularly most prominent resuscitative drug for more than a century and for good reason It improves the success of initial resuscitation with the likelihood of restoring spontaneous circulation In experimental animals, it has been shown to increase survival, but there is no secure evidence of survival benefit in human patients Unfortunately, the same applies to vasopressins Theoretically, vasopressin has advantages over epinephrine in that it may diminish the severity of postresuscitation myocardial dysfunction, especially in patients with ischemic heart disease, in whom beta adrenergic blockade has reduced the risk of fatal ischemic episodes There is experimental evidence of protection by the administration of a beta adrenergic blocking agent during CPR Hence, there has been interest in alternative non-adrenergic vasoconstrictor drugs, including angiotensin II, endothelin for which no secure data of benefit exist, and arginine vasopressin At the time of this writing, vasopressin has advantages over epinephrine, but there is no secure proof that any vasopressor drug improves long-term outcomes With respect to bicarbonate or other buffer agents, there is no persuasive evidence of improved outcomes but instead the potential of serious adverse effects Drug management of arrhythmias Two dicta emerge The first is that the routine administration of any antiarrhythmic drug during CPR has not been 811 812 M.H Weil and W Tang proven to increase long-term survival The second is that almost all antiarrhythmic drugs are also proarrhythmic Of all agents currently available, amiodarone remains the best option for drug management of recurrent ventricular tachycardia and ventricular fibrillation other than those due to electrolyte abnormalities Admittedly, no survival benefit beyond hospital discharge has been demonstrated There is now no secure evidence favoring the administration of lidocaine, bretylium, and procainamide Administration of atropine, though still widely practiced for management of bradyarrhythmias or agonal rhythms, also has no proven survival benefit Accordingly, present data prompt us to conclude that antiarrhythmic agents, like other routine pharmacological interventions, have so far failed to improve outcomes of sudden death Moreover, these drugs unfortunately have the potential for serious adverse effects Hypothermia was widely used in conjunction with cardiac surgery in the 1950s and later in conjunction with cardiopulmonary bypass The recent demonstration that modest hypothermia in the range of 32ºC to 35ºC produces impressive improvement in neurological outcomes has prompted widespread enthusiasm for its routine use The rationale for its use, and especially the pioneering of the late Peter Safar, have established both the rationale and benefits of its routine use As yet, however, there is need for agreement on preferred methods of cooling, methods of monitoring core temperature, and the rationale for and interpreting measurements such as blood gases during hypothermia Prevention of adverse effects of hypothermia, including thrombocytopenia and platelet dysfunction, which compromises blood clotting, is being actively explored Complications include cold diuresis, hypernatremia with hyperosmolal states, probable pancreatic dysfunction with increases in serum amylase and hyperglycemia, and decreased insulin effectiveness The risks of infection, especially pneumonia and wound infections, are increased Better understanding of these complications is sought as a basis for patient selection The technique is promising and important The goal is to mitigate the devastation that follows irreversible ischemic injury to the brain and major neurological deficits after successful initial resuscitation pulses, especially by non-professional providers Accordingly, the pulse check is appropriately deleted from the armamentariam of the BLS provider Even for the professional provider, it is unlikely that palpation is reliable, especially during uninterrupted chest compression Most important, however, is the consensus that chest compression should not be delayed for a pulse check The possibility that the presence or absence of the heart beat may be detected by measurements of transthoracic impedance is attractive The most consistent guide for predicting the likelihood of defibrillation and restoration of spontaneous circulation is the coronary perfusion pressure (CPP) Except for patients who are invasively monitored in the hospital prior to cardiac arrest in the operating suite, cardiac catheterization laboratory, or intensive care unit, this is not applicable in other settings and especially out-of-hospital End-tidal PCO2 (EtPCO2), however, is an excellent surrogate of both coronary perfusion pressure and cardiac output generated by chest compression.12 EtPCO2 is also useful for guiding effective chest compression and for the decision to discontinue CPR Chest compression should consistently increase and maintain EtPCO2 at levels exceeding 15 mm Hg Although there are only observational clinical data to secure the proposed rule that CPR efforts may be abandoned absent EtPCO2 values exceeding 10 mm Hg for more than 10 minutes in normothermic patients, this deserves consideration Pulse oximetry fails during cardiac arrest when peripheral blood flow is critically reduced or ceases Measurements of cardiac output and oxygen consumption during CPR are both impractical and of no proven value Blood gases, oximetry, serum electrolytes, and arterial blood lactate are potentially useful measurements including detection of carbon monoxide intoxication, life-threatening hypoglycemia, some drug intoxications, and electrolyte abnormalities Sublingual tissue CO2 is also of unproven value for guiding cardiac resuscitation Nevertheless, each of these measurements is of substantial value primarily for postresuscitation management rather than during CPR There are important advances in the search for a predictor to guide the timing and predict the success of a defibrillating shock.12 These include electrocardiographic measurements based on voltage (amplitude), frequency, and an algorithm that represents a combination of amplitude and frequency (AMSA) Monitoring and measurements Thrombolysis It is clear that the detection of cardiac arrest cannot be achieved reliably by palpation of the carotid or femoral The therapeutic value of anticoagulants and thrombolysis in settings of acute myocardial ischemia and following Postresuscitation care Bringing it all together pulmonary embolization is undisputed There is also evidence of impaired microvascular blood flow with stasis during and following resuscitation from cardiac arrest The potential value of anticoagulants and of thrombolytic agents that have proteolytic activity acting on prothrombin and thrombin in settings of CPR have been based on experimental data, but as yet have gained no clear clinical support Observational studies project a five-fold greater likelihood of bleeding including intracranial hemorrhage The incidence of serious bleeding is only 3%, however, which is best viewed in relation to the current national estimate of greater than 95% overall mortality after outof-hospital cardiac arrest Though the rationale for anticoagulants and thrombolysis is conceptually attractive, clinical data are insufficient to support its use as adjunctive therapy during CPR at this time In-hospital resuscitation The overall survival is largely contingent on co-morbidities Better outcomes are likely if preventive measures are instituted by which the incidence of cardiac arrest is reduced Proactive Medical Emergency Teams (METs) have been organized to identify patients at risk, arrange prompt transfer of such patients to more intensive observation and management in monitored beds, or transfer into intensive care units The success of the MET, the organized early response team, which typically includes a Critical Care or Emergency Medicine specialist and a Critical Care/Emergency Medicine RN specialist, is likely to be contingent on the local hospital setting There is lesser need in teaching hospitals and greater benefit in non-teaching hospitals in the absence of in-house physicians Hospitalists increasingly provide in-house services, including MET equivalents The effectiveness of a MET is also contingent on the geographic location of patients and availability of monitored beds Finally, much is determined by the culture of the institution and the extent to which physicians and other health providers share responsibility without undue fear of intrusion or perceived liabilities A special issue relates to the perceived obsolescence of manual defibrillators that not deliver biphasic waveform, lower energy shocks, and escalating energies up to 360 joules The likelihood that such compromise outcomes is now of lesser concern, however The new and now more appropriate routine is delivery of only one shock with brief interruption of chest compressions A single shock will therefore be at the lowest power setting, typically 200 joules Complications As yet unsettled are the possible benefits and the adverse effects of the “precordial thump” delivered after witnessed cardiac arrest There is persuasive evidence that a mechanically induced chest wall impact so timed that it immediately precedes the peak of the T wave may induce ectopic ventricular arrhythmias including ventricular fibrillation, so-called COMMOTIO CORDIS Defibrillation produces skin burns, the so-called perimeter effect.13 Electrical shocks produce increases in both total creatine phosphokinase (CPK) principally from striated muscle and in the cardiac CPK-MB fraction together with Troponin T of myocardial source If the rescuer is shocked, it is an unpleasant experience but quite remarkably, there has never been documentation of serious injury In a majority of victims, manual precordial compression fractures ribs This applies also to mechanical chest compression, including the LUCAS® and the Autopulse®, together with a minority incidence of sternal fractures In contrast to primary cardiac causes of cardiac arrest in older adults, the predominant causes of cardiac arrest in pediatric patients are not cardiac They are associated with asphyxia and especially foreign body aspiration and drowning or traumatic blood loss with exsanguination More recent experimental studies nevertheless provide persuasive evidence that opening the airway and starting ventilation not alone result in optimal outcomes After onset of cardiac arrest, conventional precordial compression would best be part of initial management Ventricular fibrillation occurs in fewer than 10% of pediatric patients If VF evolves during resuscitation from pulseless rhythms or asystole, the likelihood of a favorable outcome is diminished The empirical decision to “dose” the energy delivered at joules/kg proves 90% effective Newer versions of AEDs that deliver biphasic waveform shocks provide pediatric cables and electrodes that attenuate the delivered shock to between 50 and 80 joules, an appropriate dose for children The routine of airway intubation for pediatric patients with cardiac arrest in out-of-hospital settings has been largely abandoned because of the dual detriments of delayed ventilation and precordial compression and the high incidence of both airway trauma and esophageal intubation As in adults, substantially lower tidal volumes are now delivered to avoid hyperventilation Also as in adults, there is currently no proof that routine administration of drugs is of proven value Calcium gluconate or chloride is administered on specific indication, including calcium channel blockade overdose, hyperkalemia, and hypocalcemia 813 814 M.H Weil and W Tang Sodium bicarbonate is administered for management of hyperkalemia and tricyclic antidepressant overdose Vascular access is now most predictably obtained by the intraosseous route Neurological recovery is compromised by fever We anticipated major benefits of hypothermia, but for pediatric patients additional objective clinical confirmation is awaited In pediatric patients who sustain cardiac arrest after cardiac surgery, early implementation of extracorporeal oxygenation (ECMO) has survival value REFERENCES Concluding comments Though a preponderance of controlled clinical studies have failed to establish survival benefits, especially for drugs, the absence of proven benefit is not to be interpreted that there is no potential for benefits There are extraordinary ethical and legal limitations that typically impose serious restraints on the enrollment of patients during cardiac arrest, and equally formidable challenges in the implementation of such human experiments Accordingly, we must not despair of what may appear to be a see-saw of progress, but maintain appreciation and optimism for the progress that is being achieved 10 11 12 13 II Kings, Chapter 4, verses 34-35, Bible, King James Version Weil, M.H & Tang, W Cardiopulmonary resuscitation: A promise as yet largely unfulfilled Disease-a-Month 1997; 43(7): 429–504 Weil, M.H., Tang, W & Bisera, J Cardiopulmonary resuscitation One size does not fit all Circulation 2003; 107: 794 (Editorial) Nolan, J.P & Gabbott, D.A Airway techniques and airway devices, Chapter 29, this volume Kerz, T., Paret, G & Herff, H Routes of drug administration, Chapter 33, this volume Idris, A.H & Gabrielli, A The physiology of ventilation during cardiac arrest and other low blood flow states, Chapter 28, this volume White, R.D., Colqhoun, M., Davies, S., Peberdy, M.A & Timerman, S Public access defibrillation, Chapter 27, this volume Weisfeldt, M.L & Becker, L.B Resuscitation after cardiac arrest A 3-phase time-sensitive model J Am Med Assoc 2002; 288: 3035–3038 Cobb, L.A Sequence of therapies during resuscitation: defibrillation vs compressions, Chapter 24, this volume Kohli, P & Greenland, P Role of the metabolic syndrome in risk assessment for coronary heart disease J Am Med Assoc 2006; 295: 819–821 Campbell, C., Gluckman, T., Henrikson, C., Ashen, D & Blumenthal, R Prevention of sudden cardiac death, Chapter 23, this volume Ward, K.R & Bisera, J Cardiac arrest resuscitation monitoring, Chapter 38, this volume Baubin, M., Rabl, W & Hoke, R Complications of CPR, Chapter 45, this volume ... reproduction of any part may take place without the written permission of Cambridge University Press First published in print format 2007 eBook (EBL) ISBN -1 3 97 8-0 - 51 1-3 548 9-2 ISBN -1 0 0-5 1 1-3 548 9-4 eBook. .. (EBL) ISBN -1 3 ISBN -1 0 hardback 97 8-0 -5 2 1- 8 470 0 -1 hardback 0-5 2 1- 8 470 0 -1 Cambridge University Press has no responsibility for the persistence or accuracy of urls for external or third-party internet... Cardiac Arrest The Science and Practice of Resuscitation Medicine Second edition Cardiac Arrest is the definitive and most comprehensive reference in advanced life support and resuscitation medicine