EMAC Participants Manual 2010-1

EFFECTIVE MANAGEMENT OF ANAESTHETIC CRISES
PARTICIPANT MANUAL
SECOND EDITION 2010
ANZCA
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EMAC
EFFECTIVE MANAGEMENT OF ANAESTHETIC CRISES SECOND EDITION 2010
Editor
Assoc Prof Sandy Garden FANZCA
Contributors
Assoc Prof Brendan Flanagan FANZCA Assoc Prof Sandy Garden FANZCA Dr Tim Gray FACEM Dr Stuart Marshall FANZCA Dr Richard Morris FANZCA Dr Adam Rehak FANZCA Assoc Leonie Watterson FANZCA Assoc Prof Jennifer Weller FANZCA
Acknowledgement
Assoc Prof Brian Robinson PhD (proof-reading)
AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS

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Published in 2010 by Australian and New Zealand College of Anaesthetists, 630 St Kilda Road Melbourne Victoria 3004 Australia
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CONTENTS
INTRODUCTION TO FIRST EDITION ......................................................................................................... VI INTRODUCTION TO SECOND EDITION ................................................................................................... VII HUMAN PERFORMANCE ISSUES ................................................................................................................... 1 OVERVIEW ........................................................................................................................................................... 1 GENERIC PRINCIPLES FOR PREVENTION & MANAGEMENT OF DIFFICULT CLINICAL SITUATIONS ........................ 5 GABAS SEVEN KEY POINTS FOR PREVENTING & MANAGING CRITICAL EVENTS ............................................ 5 PERFORMANCE-SHAPING FACTORS, INCLUDING PRODUCTION PRESSURE ........................................................... 8 TEAMWORK ISSUES: SOCIAL PSYCHOLOGY OF THE OPERATING THEATRE ....................................................... 12 SUMMARY ......................................................................................................................................................... 13 CARDIOVASCULAR EMERGENCIES .......................................................................................................... 15 OVERVIEW ......................................................................................................................................................... 15 MYOCARDIAL ISCHAEMIA & ACUTE CORONARY SYNDROMES.......................................................................... 16 CARDIAC ARREST & POST-ARREST CARE ......................................................................................................... 19 CARDIOVERTER/DEFIBRILLATORS ..................................................................................................................... 29 CRISES WITH VALVULAR HEART DISEASE ......................................................................................................... 32 HYPERTENSIVE CRISES ...................................................................................................................................... 33 PERIOPERATIVE STROKE .................................................................................................................................... 33 EMERGENCY VASCULAR ACCESS ...................................................................................................................... 33 AIRWAY EMERGENCIES ............................................................................................................................... 37 OVERVIEW ......................................................................................................................................................... 37 THE PRIMARY PLAN FOR AIRWAY MANAGEMENT ............................................................................................ 38 CONTINGENCY PLANS ....................................................................................................................................... 41 EMERGENCY PLANS ........................................................................................................................................... 44 UPPER AIRWAY OBSTRUCTION .......................................................................................................................... 45 IMPAIRED GAS EXCHANGE ASSOCIATED WITH A PATENT AIRWAY .................................................................. 49 SUMMARY ......................................................................................................................................................... 50 APPENDIX 1 : DIFFICULT AIRWAY SOCIETY ALGORITHMS ................................................................................ 51 APPENDIX 2 : SURGICAL AIRWAY ANATOMY ................................................................................................... 54 ANAESTHETIC EMERGENCIES ................................................................................................................... 59 OVERVIEW ......................................................................................................................................................... 59 AN IMMEDIATE RESPONSE TO A CRISIS ............................................................................................................. 60 DEVELOPING SKILLS IN A WORKING TEAM ....................................................................................................... 60 BEHAVIORAL STRATEGIES TO IMPROVE DIAGNOSIS .......................................................................................... 61 A SYSTEMATIC APPROACH TO CRISIS MANAGEMENT ....................................................................................... 62 SUMMARY ......................................................................................................................................................... 63 APPENDICES ...................................................................................................................................................... 64 THE MANAGEMENT OF TRAUMA .............................................................................................................. 70 OVERVIEW ......................................................................................................................................................... 71 INITIAL MANAGEMENT ...................................................................................................................................... 71 PRIMARY SURVEY ............................................................................................................................................. 71 RESUSCITATION ................................................................................................................................................. 72 SECONDARY SURVEY ........................................................................................................................................ 72 EVOLVING INJURIES........................................................................................................................................... 73 HAND-OVER OF CARE ........................................................................................................................................ 73 MANAGEMENT OF LARGE-VOLUME RESUSCITATION ......................................................................................... 73 ANAESTHETIC IMPLICATIONS OF AIRWAY TRAUMA .......................................................................................... 74 ANAESTHETIC IMPLICATIONS OF CHEST TRAUMA ............................................................................................. 76 INTRA-CRANIAL TRAUMA .................................................................................................................................. 76 X-RAYS IN THE TRAUMA SETTING .................................................................................................................... 77
Introduction to First Edition

The Concise Oxford Dictionary defines effective as actually useful. Crisis comes from the Greek krisis meaning decision and is defined as time of danger or as a time of decision. Effective Management of Anaesthetic Crises (EMAC) is a course intended to provide practical techniques in the management of anaesthetic emergencies. Anaesthesia alone could be described as a time of danger. In no other human activity are seemingly healthy individuals rendered unconscious, paralysed and deprived of their usual respiratory or cardiovascular control mechanisms. The anaesthetist takes over the decision making from the individuals homeostatic control centres. The onset of danger is relative to a threshold. This could range from when one physiological variable falls outside the healthy range to when the anaesthetist cannot simultaneously administer the drugs on behalf of the vasomotor centre, monitor end-tidal gases for the respiratory centre and put in a necessary central line. This course does not establish these thresholds; they are dependent on many factors and beyond the scope of a two and a half-day course. Instead, EMAC focuses on how a crisis can be recognised and subsequently managed. The aviation industry has recognised that simply knowing what needs to be done in an emergency may not avoid disaster and specific training in how to deal with emergencies is now standard practice. Throughout training, anaesthetists are taught many anaesthetic skills and on completion of their fellowship have a thorough knowledge of what must be done in an emergency. EMAC follows the lead made in other industries and focuses on how anaesthetists can utilise their existing knowledge and enable this knowledge to be applied effectively in a crisis. EMAC brings a significant new approach to medical training that emphasises the behavioural aspects of managing anaesthetic crises. Effective management of emergencies, particularly in aviation, is now recognised to hinge on the behavioural aspects of leadership and the interaction with a team. There is growing recognition that the surgical and anaesthetic staff in an operating room similarly work as a team, particularly during emergencies. EMAC focuses on the role of the anaesthetist as the leader of this team during an anaesthetic crisis and the interaction with the people around the anaesthetist to use their skills and resources effectively. In addition, this course develops the behavioural strategies to facilitate decision making and encourages the use of protocols during anaesthetic emergencies. Brian Robinson February 2001
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Introduction to Second Edition

The EMAC Course represents an on-going endeavour by a group of medical and nonmedical experts who are committed to improving the management of crises in the domain of anaesthesia as well as in other domains of acute patient care. The course materials represent the expert opinion of the authors and those who attended a series of editorial workshops held during 2009. As such the teaching materials represent the opinions are those individuals, rather than the opinion of ANZCA. A number of illustrations have been reproduced in these manuals within the terms of ANZCAs Education Licence. ANZCA thanks the original authors and publishers who allowed these materials to be reproduced. As the President of ANZCA, I thank all those who have contributed to the evolution of this course and these educational materials, particularly those who wrote these materials. Leona Wilson President Australian and New Zealand College of Anaesthetists. January 2010
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Human Performance Issues

Dr Stuart Marshall Assoc Prof Brendan Flanagan
This module aims to increase understanding of the various means by which the performance of anaesthetic practitioners - as individuals and as part of a health care team - can impact on patient care. Objectives Understand the psychology of human performance in anaesthesia Understand generic principles of crisis prevention and management Recognise performance-shaping factors, including production pressure Understand the concept of a systems approach to patient safety Incorporating new technologies. Introduction of standards & guidelines. Addressing problems relating to human factors and system issues. Despite these changes, the domain of the anaesthetist remains very challenging. Anaesthesia continues to be a unique specialty in terms of the common occurrence of conditions that challenge optimum human performance. The anaesthesia practitioner must perform almost flawlessly despite: Less than ideal environmental conditions such as poor light, noise, or ambient temperature. Distractions, such as alarms and multiple tasks. Often conflicting objectives with inadequate information available to support optimal decision-making. The aim of this module is to increase understanding of the significance of the performance of the anaesthetist - as an individual and as part of a team - on patient care. Increased awareness of these issues may impact positively on patient care and outcome. We hope to draw on your experiences to enable us all to gain new insights into these matters.
Overview
Why Focus on Human Performance Issues?
There has been an explosion of interest in the issue of human performance in high-risk industries during the past 5-10 years. As hardware and software solutions have become more reliable, the human contributions to safety have become ever more apparent 1 p1. Anaesthesia is acknowledged as the leading medical specialty in addressing issues relating to human performance in healthcare, and in patient safety initiatives in general. Some of the strategies that anaesthesia has introduced include:
Firstly, what are the pros & cons of having humans involved in the system of delivery of anaesthesia? Human beings are not machines. When maintained, machines are generally very predictable and reliable, whereas humans are unpredictable and unreliable, and our ability to process information is limited by the capacity of our (working) memory. However, in regard to decision-making, the performance of human beings is incredibly creative, flexible and powerful - in ways that no computer can match. Conversely, human performance is vulnerable to distractions, biases and errors. Distractibility is both a strength and a weakness. It helps us notice when something unusual is happening, and we are very good at recognising and responding to situations rapidly, and adapting to new situations and new information. But our ability to be distracted also predisposes us to error, because when distracted we may not pay attention to the most important aspects of a task or situation. Our brain can also play tricks on us, by misperceiving a situation one of the main reasons that making errors is a fundamental and inevitable feature of the human condition. Humans are very poor at multi-tasking, that is trying to concentrate on and perform more than one task at a time however computers are very good at this! Humans possess the big advantage of being able to recall past experiences in order to perceive a problem and develop a solution. By comparison, current computers can only deal with situations for which they have been programmed (by humans!). However, machines (computers) never get tired, always do things the same way and do not suffer from bias in association with previous experience! In summary, human factors psychologists agree that optimum performance in complex, dynamic fields such as anaesthesia requires an appropriate combination of man and machine. A fundamental premise underlying the rationale for this module is that To Err is Human. In fact this is the title of a landmark patient safety document released in the U.S.A. in December, 1999 and which has led to sweeping changes in the way that patient safety is perceived in health-care. The reality that humans err, results from the physiological & psychological limitations of
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human performance. Contributors to error include: Fatigue Workload Fear of blame Mental overload Poor interpersonal communications Imperfect information processing Flawed decision-making Unfortunately, doctors tend to overestimate their ability to function flawlessly under adverse conditions, such as under the pressures of time, fatigue, or high anxiety. An important consideration is that the problem of medical error is not fundamentally due to lack of knowledge. Many adverse events in medicine result from actions made by persons who know how to perform the relevant task safely, have done so many times in the past - and face significant personal consequences of the action! We will explore some of these issues in more detail in this module.
Individual Performance
Psychology of Human Performance in Anaesthesia This section is predominantly a distillation of the introductory section from Crisis Management in Anesthesiology 2 and has been undertaken with the permission of the authors. You are strongly encouraged to read the first two chapters of that book and the more recent and related Chapter 83 in Millers Anesthesia 3 . The practice of anaesthesia is a complicated collection of mental and physical activities attuned more to the efficient care of routine cases than to the handling of life-threatening crises. How newcomers to anaesthesia become skilled practitioners is only recently beginning to be understood, and the fundamental question of what is meant by expertise in anaesthesia is only now starting to be explored. Experience of challenging situations plays a significant role in the development of expertise as does, it is theorised, deliberate practice afforded by exposure to simulated emergencies. Despite this we have discovered that initial training and continuing education often leave substantial gaps in the ability of
some anaesthetists to deal with crises. When a critical incident does occur, it is apparent to everyone who works in an operating theatre that some anaesthetists cope better than others. They are the ones who can restore order in the midst of chaos, who know what to do, and how to get it done. They can make and execute good decisions and manage people. In short, they are the ones we would want to give our anaesthetic! Why are some seemingly better than others at this, and can these skills be learned and taught? As a specialty we are only beginning to examine these issues, perhaps because until recent times we have erroneously thought of anaesthesia practise in terms of more traditional forms of medicine. In fact, some of the dominant features of our work complexity, uncertainty, time-pressure, dynamism (i.e. things can happen very quickly sometimes!) - share more in common with industries such as aviation, nuclear power and fire-fighting than they do with other forms of medicine. We are beginning to understand the mindset of the anaesthetist better by looking at research findings from these other fields. In fact there are several successful safety strategies in aviation that could be incorporated into anaesthesia, though this has yet to happen systematically. These include: Use of written checklists to help prevent crises from occurring e.g. anaesthesia machine checklist. Use of established procedures (both memorised & written), for responding to crises e.g. algorithms 4. Training in decision-making & operating team co-ordination. Systematic practice in the handling of crisis situations (including the use of immersive simulation training). Anaesthetists who adopt many of these strategies will enhance patient safety through improved performance. The remainder of this section is intended to provide an introduction to the psychological issues involved in optimal performance by anaesthetists. Anaesthetists are required to make both routine
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and complex decisions regarding patient care during the intraoperative period. There is also a variety of tasks with varying degrees of complexity that need to be performed. Expert performance in anaesthesia involves a repeated loop of observation, decision, action & reevaluation. Gaba describes the anaesthetists mental activities operating at several levels almost simultaneously. At a sensorimotor level, activities involving sensory perception or motor actions take place with minimal conscious control, e.g. squeezing the bag to ventilate the patient. At a procedural level, the anaesthetist performs regular subroutines that have been derived from previous work episodes, e.g. switching to 100% O2 and from ventilator to hand ventilation in response to a falling O2 saturation. A level of abstract reasoning is used primarily in unfamiliar situations for which no well-practiced expertise is available from previous encounters. e.g. thinking through the causation & management of refractory hypotension Supervisory control is concerned with dynamic allocation of the anaesthetists finite attention to routine and non-routine actions, e.g. using a regular systematic scanning process to ensure nothing is being missed. Resource management occurs at the highest level of mental activity and deals with the command and control of all available resources, i.e. the ability to translate the knowledge of what needs to be done into effective team activity. These last two levels involve dynamic adaptation of the anaesthetists own thought processes. This ability to think about ones own thinking in order to strategically control ones own mental activities, is called metacognition and is a very important part of successful crisis management and up until now has not been part of traditional training. The following points warrant consideration: Observation: Management of dynamic situations depends on the anaesthetists responses to many sources of rapidly changing information. But the human mind can only attend closely to one or two items at a time. In
fact the anaesthetists attention is such a scarce resource that its allocation is extremely important in nearly every aspect of dynamic decision-making. Vigilance, the capacity to sustain attention, is a necessary, but in itself insufficient, component of decision-making and crisis management. Human beings tolerate boredom poorly, making it very difficult to maintain vigilance during periods of low or monotonous workload or prolonged inactivity. Verification: Knowing when and how to verify data is another important metacognitive skill. For instance, the anaesthetist must decide under what conditions it is appropriate to invest time, attention and energy on establishing a new form of monitoring, such as placing a pulmonary artery catheter in the middle of a case, as opposed to relying on more indirect monitoring already in place. Problem Recognition: Problem recognition involves matching sets of data to patterns that are known to represent specific types of problems. Unfortunately the available data streams do not always disclose the existence of a problem, and even when a problem is detected, the cues often do not specify its nature or cause. Therefore, when a clear-cut match or diagnosis cannot be made, anaesthetists use approximation strategies, termed heuristics, to handle these ambiguous situations. One of the most common of these is so-called frequency gambling choosing the single most likely event as the diagnosis. This approach is a two-edged sword. Frequency gambling on expected problems can seriously derail problem solving when the gamble does not pay off that is, when the diagnosis is not correct. The anaesthetist may then persist with solving the incorrect problem even when the evidence is clear that the diagnosis is incorrect - a situation termed fixation error (see below). Precompiled Responses: The initial responses of experts to most perioperative events arise from precompiled responses - plans for dealing with the specific type of event - so-called recognition-primed decision making. However even optimised responses are destined to fail when the problem is not due to the suspected aetiology or when it does not respond to the usual actions one of the many reasons why performing anaesthesia by cookbook is undesirable.
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Co-ordination of Activities via Supervisory Control: During the administration of anaesthesia, not only are there a plethora of tasks to perform, but these tasks can periodically generate so much mental workload that the anaesthetists ability to respond to other events is degraded (e.g. focusing so much on correct placement of the endotracheal tube that worsening hypoxia is not recognised). The key component of crisis management in such a situation is the anaesthetists ability to modulate their own thinking through supervisory control and resource management. The supervisory controller allocates the scarce resource of attention during multitasking. Action Implementation: A particular feature of the practice of anaesthesia, unlike other branches of medicine, is that the decision maker does not just writes orders, but is also directly involved in the implementation of actions (such as administering medication). Executing these actions requires substantial attention and may impair the anaesthetists physical ability to perform other activities (e.g. having to give a drug while putting in a central venous catheter). In performing actions a variety of errors of execution, termed slips, may occur. These are actions that do not occur as planned, e.g. turning the wrong switch or making a syringe swap. Re-evaluation: Successful dynamic problem solving during a state of uncertainty requires the supervisory control to initiate frequent reevaluation of the situation. Re-evaluation returns the anaesthetist to the observation step, but with specific assessments in mind. In relation to the efficacy of any interventions: Is the problem getting better, are there any new problems, and was the initial diagnosis correct? Resource Management: This concept, borrowed directly from the world of aviation, encompasses the ability of the anaesthetist to command and control all the resources at hand in order to execute the anaesthetic as planned and to respond to problems that arise. This is the ability to translate the knowledge of what needs to be done into effective team activity in the complex and ill-structured real world of the operating theatre.
Generic Principles for Prevention & Management of Difficult Clinical Situations

The decisions and actions taken by anaesthetists can contribute to the outcome of the patient's surgery. Even for elective surgery in ASA I patients, there is an ever-present (albeit small) risk of catastrophe. Death, brain damage, or other permanent injury is the endresults of many pathways that can begin with fairly innocuous triggering events. Each intervention, even if appropriate, is associated with side effects, some of which have the potential to be catastrophic. Furthermore, many risks cannot be avoided. Although the old adage still holds true (it is easier to stay out of trouble than to get out of trouble), even the most skilled anaesthetist can find their talents challenged in the operating theatre today. All over the world, improved anaesthesia care has meant that sicker patients present for surgery - yet when problems occur, our actions can come under intense scrutiny. Expectations are very high among our patients and surgical colleagues. A crisis is "a time of great danger or trouble whose outcome decides whether possible bad consequences will follow (Gaba). Notice that in this definition, blame is not placed for the development of a crisis. There are so many factors that impact on the management of a patient that are beyond the anaesthetists control that there does not have to be an error made for a crisis to occur. However, understanding more about the ways in which crises develop may help us to prevent/avoid these events, and prevention/avoidance of such events is implicit in the principles of crisis management. For our purposes a crisis or "the time of great danger" is typically a brief, intense event or sequence of events that offer a clear danger to the patient requiring an active response to ameliorate patient injury. A crisis is often perceived as being sudden in onset and rapid in development but at least in retrospect one can often identify an evolution of the crisis from underlying triggering events. Indeed the combination of the complexity and the dynamism of the environment make crises more likely to occur in fields such as anaesthesia (and intensive care and emergency medicine). But the skills required to manage
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the entire situation of the crisis have not received a great deal of attention in the formal training of anaesthetists until recent times. To safeguard the patient, the anaesthetist must manage the entire situation of the crisis, including the environment, the equipment, and the patient care team consisting of the surgeon, anaesthetist, nurses and technicians. Skilled crisis management requires that the anaesthetist, while under stress and time pressure, optimally implements standard techniques of diagnosis and treatment. Medical knowledge and skills, while essential components, are not enough.
Gabas Seven Key Points for Preventing & Managing Critical Events
Several basic principles may help manage a crisis more effectively, especially as humans arent very good at decision-making under pressure.
1. Know, Modify & Optimise Your Environment

Establish the location and procedures for using emergency equipment and supplies. Is the layout of your (potentially new) work environment conducive to optimal management of a current, or potential, emergency situation? If not, can the layout be changed (including the position of the anaesthetic machine and drug cart in relation to the OR table)?
2. Anticipate & Plan

The best way to avoid a crisis is to not have one. Failure to prepare for a situation/procedure is one of the most frequent contributions to errors and mishaps. Be sure you have accumulated sufficient information about the patient, procedure, equipment and drugs. Do you know how to access emergency supplies and other resources? The best use of resources requires advance planning. Appropriate plans come in three forms: -Global plans for resource mobilisation in a specific work environment. -Specific plans for dealing with particular problems of a specific situation (see Runciman et als crisis management
algorithms 4). -Generalised emergency procedures for the management of critical incidents. While it may be unstated, specific backup procedures and contingency plans should be formulated, in case the original plans fail. In other words, plan for the worst-case scenario.
5. Call for Help or a Second Opinion Early Enough

Anaesthetists have a tendency to put off calling for help. When information seems confusing, or you feel you are operating beyond safe or healthy limits of your ability to assimilate data or to physically accomplish necessary functions, have a reasonably low threshold for asking for assistance - it is easy to get into a situation where it is impossible to manage all that needs to be done. Importantly fresh help may see things that the initial person on the spot has missed. Remember that help may not arrive immediately, depending on the circumstances, so dont wait too long to call.
3. Ensure Leadership and Role Clarity

Someone has to manage the overall operating room team. In most emergency situations that should be the anaesthetist. Make sure that this does occur, and that leadership is clear to the other members of the team. What does it mean to be a Leader? Firstly it is a matter of recognising that there needs to be a leader and declaring who IS to be the leader! Then it is primarily a matter of directing and coordinating the team tasks, i.e. deciding what needs to be done, prioritising the necessary tasks, and assigning them to specific individuals. The anaesthetist in charge of the situation must have good technical knowledge and skills and must remain calm and organised. This command authority is vital to maintaining control of the situation, but control should be accomplished with full participation of the team. The leader should be the clearinghouse of information and suggestions from other team members. Sound leadership is aided and abetted by good followership, such that other members of the team (surgical & nursing) are able to convey assertively information that may be vital to the management of the situation.
6. Allocate Attention Wisely & Use All Available Information Avoid Fixation Errors
Errors are possible during routine situations, and even more likely during the management of a critical event. A common type of error is called a fixation error, which is an undue persistence in failing to revise actions in the face of readily available contradictory information. One of the better-established (yet often overlooked) findings in stress research is that as stress levels increase, an individuals thought processes and breadth of attention narrow (termed attentional or cognitive tunnelling) so that fixation (on only one facet of the evolving situation) is more likely. This is an important reason for calling for help if you are stressed you are probably missing something!
4. Communicate Effectively
Let others within the team know when a situation is developing. Give clear specific instructions to those you are managing. Dont be vague. Dont speak into thin air. Call people by their names, use eye contact and gesturing to help identify people. Encourage feedback. Encourage others to close the communication loop, i.e. they need to answer your clear communication with an equally clear communication, signalling that they understand your directive. An open communication style also enables the team members to feedback when the task is completed, to proactively help the leader, and offer suggestions.
Figure 1. Attentional tunnelling. In a crisis or times of stress, the tendency is to focus on one variable or explanation to the exclusion of others (from Endsley et al, 2003).
7. Distribute the Workload & Use All Available Resources

Designate tasks to those who can best do them. You have many resources: yourself, your anaesthetic assistant, the surgeon, other nurses and technical personnel, and other anaesthesia personnel. Direct your team members effectively. Resources such as monitors and alarms can be optimised to help reduce workload. Humans are poor at vigilance tasks, and alarms are useful adjuncts to the anaesthetists limited attention span.
To avoid these kinds of error, use your second opinion, frequently re-evaluate what you are doing and maintain situation awareness. That is, strive to constantly keep the big picture in mind!
Situation Awareness
Experts seem to be able to grasp the importance of every detail in the midst of the mass of information presented during a crisis (Figure 2). They seem to have eyes in the back of their head or the right stuff because they are able to establish and maintain what cognitive psychologists call situation awareness.
Fixation Error
There are three main types of fixation error that should be carefully understood: This and only this Persistent failure to revise a diagnosis or plan, despite plentiful contradictory evidence. The available evidence is interpreted to fit the initial assessment of the situation. Attention is allocated to a minor aspect of a major problem. Everything but this Persistent failure to commit to the definitive treatment of a major problem. an extended search for information is made without ever addressing potentially catastrophic conditions. Everything's OK Persistent belief that no problem is occurring in spite of plentiful evidence that it is. Abnormalities are attributed to artefacts or transients (pulse oximeter is a classic!). Failure to declare an emergency or accept help when facing a major problem.
Figure 2. Good information acquisition in a crisis. Large volumes of information are assembled into a picture of the situation (from Endsley et al, 2003).
Situation awareness has been defined as the perception of elements in the environmentthe comprehension of their meaning and the projection of their status in the near future (Endsley 1988) see fig 3). Having a firm grasp of the situation as it unfolds allows the leader to compare it to their expectations and revise their actions accordingly.
Figure 3. Situation awareness is the perception of elements in the environmentthe comprehension of their meaning and the projection of their status in the near future (Endsley, 1995). 7
outcome. The concept of situation awareness has evolved from aviation research to address the important role that human performance plays in adverse occurrences. Analysis of accidents and near misses in aviation and now anaesthesia & critical care medicine has revealed that blind spots in the operators view of the big picture often trigger (and contribute to) the evolution of a crisis. During routine administration of anaesthesia, maintenance of a high level of situation awareness may not be all that necessary. The relative rarity of potentially catastrophic problems and the checks and balances built into the system allow lapses of attention and decision errors to occur without impact on outcome. During an emerging crisis however, the cost of failure to maintain situation awareness during the periods of low workload may become apparent. All of a sudden it seems that many things need to be done simultaneously and time and attention become precious but limited resources. If these resources are consumed, it may be impossible to recover from a deteriorating process. Once again, sorting out what is important and keeping track of it at all times are hallmarks of the expert practitioner. One of the best ways to maintain situation awareness during an evolving situation is to delegate tasks as much as possible, thus freeing yourself up to keep an eye on all of what is happening. There are several performance-shaping factors that are potentially of sufficient magnitude to be of concern to the anaesthetist hence it is worthwhile being aware of the following issues in relation to our day-to-day work, especially if more than one of these factors are occurring simultaneously (e.g. illness & fatigue). Ultimately the responsibility rests with the anaesthetist to ensure his/her performance level is sufficient for the work at hand. A major difficulty is that organisations rarely provide mechanisms for personnel to excuse themselves if they are temporarily impaired. Ironically in many settings, mechanisms for dealing with serious problems like addiction are more established than for more common occurrences (such as illness or fatigue).
Ambient Noise
The operating theatre is a relatively noisy work environment, with mean sound levels higher than in most offices and peak levels that can be very high. While some ambient noise is controllable (conversation, music), there are some sources of noise that are inevitable and uncontrollable (surgical drills, equipment alarms). There is evidence that noise can adversely affect human performance. Operating theatre noise has been shown to interfere with speech discrimination and psychometric tests of mental efficiency & short-term memory of anaesthesia trainees. The potential for noise to interfere with the detection of audible alarms and effective communication is of particular concern. Music The use of music in the operating theatre is widespread, with an impression that it may relax the staff and enliven the day. It can even build team cohesiveness - when all team members enjoy the music! The effects of discord in relation to the choice of music may be more problematic, and some team members prefer silence during surgery. There is no simple answer to the question of the proper role of music in the operating theatre. Optimal patient care is the primary goal. The most sensible approach is to allow any team
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Performance-Shaping Factors, Including Production Pressure

The practice of anaesthesia always requires the presence of an attentive and skilled practitioner. But we are all aware that some days are better than others in relation to our ability to perform at our peak while at work. While it is unrealistic to expect peak performance in association with every anaesthetic we give, it is important to recognise that the abilities of even highly trained personnel can be profoundly influenced by internal & external performance-shaping factors. It is unclear whether the levels of performance decrement likely to be induced in typical (and indeed atypical) work situations have any significant effect on patient care &
member to veto the choice or volume of music if they believe it interferes with their work, and this is increasingly likely during periods of high workload. Masks Whilst masks are useful to prevent infection spread by droplets and splashes, they impede observation of facial expression. Studies observing communication where faces are not clearly visible have determined an increased risk of confusion. The wearing of masks makes it even more critical that communication is clear and directed, especially in crises.
adequate sleep when rostered away from work duties. Each individual has their own sleep requirement per 24-hour period. Lack of adequate sleep means daytime sleepiness and impaired performance ensue. For limited periods, performance may appear unaffected. However, short-term compensation may be due to a deliberate slowing of actions to avoid mistakes (a speed-performance trade-off), and the response to new or emergency conditions may be sub-optimal. Even minimal levels of sleep loss (2 hours less sleep than required) can lead to lapses in performance, increased physiological sleepiness and altered mood. Sleep loss is cumulative, resulting in sleep debt. The ONLY way to pay back a sleep debt is with sleep! Chronic sleep debt is commonplace in the medical culture, and research into sleep in medical staff has been hampered by the fact that chronic sleep debt is the norm. Fatigue is the diminished ability to perform work, and it is caused by excessive physical or cognitive work. Mental fatigue is accompanied by subjective feelings of tiredness after periods of sustained performance on predominantly cognitive tasks. Mood, initiative and enthusiasm all decline as fatigue progresses. Fatigue can also result from disturbed circadian rhythms. Circadian rhythms - relating to body temperature, metabolism, hormonal secretion, and the sleep/wake cycle - fluctuate on a 24-hour time scale. Circadian lulls occur twice throughout the 24-hour day - from 02:00-06:00 and 14:0018:00. These periods are associated with an increased sleep tendency and decreased performance capacity. Sleepiness & alertness are opposite ends of a continuum, with the most obvious effect of inadequate sleep being daytime sleepiness. Healthy adults are maximally alert by mid-morning. Determinants of sleepiness include: decreased quantity of sleep, decreased quality of sleep (cf. sleep apnoea), disrupted circadian rhythms, and the effects of medication, including alcohol. Long work hours, fatigue & sleep deprivation result in dramatic changes in mood and emotions. Depression, anxiety, irritability, anger & depersonalisation occur in chronically
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Reading
There are no data to determine the degree to which reading by the anaesthetist during the administration of anaesthesia distracts attention, especially if restricted to low workload periods. One positive aspect of this practice is that it may combat boredom - a significant distractor in its own right. It is probably inappropriate to ban the practice outright, but reading should not be allowed to impair vigilance or patient safety. With that in mind, a compensatory measure might be to set the patient monitor alarm limits to only a very narrow band, thereby increasing the likelihood that any deviation would be quickly noted. Of course it is to be expected that the anaesthetist must abandon all incidental activities when necessary and to have a very low threshold for abandoning any potential distractions.
Fatigue and Sleep Loss

It is likely that chronic sleep deprivation, circadian rhythm abnormalities and fatigue can be blamed for some iatrogenic adverse patient outcomes. Indeed the effect on performance of being constantly awake for 24 hours equates to a blood alcohol level above 0.05%. There is an association between the occurrence of medical incidents, performance failures, and time of day that coincides with normal sleep. However, due to the multifactorial nature of adverse events, a causal link is difficult to prove. All industries, including healthcare, are bound by Occupational Health and Safety Law to provide a safe working environment. This includes fatigue management and rostering systems that support the worker in having ample opportunities to rest. It is also the anaesthetists responsibility to ensure they get
fatigued workers. We can all relate to these issues and need to be aware of them in our interactions with patients and other staff. As mentioned earlier, vigilance, the ability to remain alertly watchful, especially to avoid danger, is important to ensure the safe passage of the patient through the perioperative period - but it is unrealistic to expect a human operator to maintain a state of peak vigilance for a protracted period of time. More important may be to learn to monitor ones own vigilance levels, recognise the onset of boredom and develop strategies to overcome it. One strategy may be a walk around the operating theatre every 15 or 30 minutes during a long procedure. Microsleeps - intermittent actual sleep episodes encroaching into periods of wakefulness, and lasting a few seconds to a few minutes - are the most extreme form of decreased vigilance. They are signs of extreme sleepiness and harbinger of sleep onset. Their occurrence is difficult to predict. Most individuals underestimate their level of sleepiness, and behavioural & subjective sleepiness can be masked by a stimulating environment. It is possible to fall asleep for a brief period and not be aware of it! Medical personnel, like anyone else, are physiologically vulnerable to degraded alertness and unable to perceive the decrement. Shift Work is an inevitable component of some forms of work, especially in the health care industry. It has been demonstrated to be associated with higher rates of alcoholism, job stress, emotional problems and physical illnesses. Ones ability to cope depends on the interaction of: Circadian rhythm. It is easier to adjust to shift changes in a forward fashion (day evening night). Social factors. Individual characteristics (such as age, personality, level of fitness). Exercise and diet. Night workers often have poor diets due to a lack of appropriate food at the workplace, and often exercise less. Personal safety Workplace fatigue is not just a problem in the workplace. Prolonged wakefulness overnight followed by a drive home can be
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dangerous a safer approach may be to find a quiet spot to nap prior to taking the trip. Countermeasures Sleep is a fundamental physiological drive that cannot be prevented by willpower alone. Because fatigue is such a widespread and insidious problem it is important to determine ways to counteract its effects. Potential countermeasures include: Scheduling patterns: Most rosters in recent years have been designed to take into account sleep requirements and circadian rhythms. As a rule rotating shifts should move in a forward direction to optimize the circadian variation. Any reasonable rostering pattern still relies on the anaesthetist to be responsible in obtaining the required amount of sleep when rostered off-duty. Education: Medical practitioners need to become more aware of the impact of sleep issues on work performance, mood, job satisfaction and health. In high risk shift patterns, monitoring of subjective scales (and even objective tests) of fatigue are warranted. Sleep hygiene: Conditions and practices that promote sufficient quantity and quality of sleep. Examples of good sleep hygiene conditions include a warm, dark, quiet room with no distractions. Rest breaks at work: Consider the role of periodic breaks to enhance vigilance, because attention spans are limited. During long cases, short breaks out of the theatre environment are helpful to clear ones mind. Strategic napping: Naps can decrease sleepiness and improve performance. Some individuals appear to benefit more from naps than others. The ideal length for a power nap is 45-60 minutes, however restorative sleep can occur with naps of only 15 minutes. Sleep inertia is a period of grogginess and reduced function for 15-30 minutes after awakening and typically occurs with naps over 1 hour of duration. Medications: Caffeine can be used to maintain alertness during periods of
extreme sleepiness, but has side-effects and can affect normal sleep. Alcohol has a soporific effect but it reduces the amount of REM sleep and is best avoided as an aid to induce sleep. Hypnotics should also be avoided, and should certainly not be self-prescribed. A short acting drug to initiate sleep may be appropriate in some circumstances but should not be taken regularly. Melatonin use is of unproven benefit in shifting the circadian cycle and is not generally available in Australia or New Zealand.
These attitudes include: "Don't tell me what to do. (Antiauthority) This guarantees repeating mistakes! "Do something quickly - anything. (Impulsivity) Acting impulsively without giving thought to the best course of action. "It won't happen to me - it's just a routine situation. (Invulnerability) Every situation could be an accident waiting to happen. Ill show I can do it. I can deal with it. (Macho) Taking chances is foolish, and increases the risk to the patient! What's the use? It's out of my hands. (Resignation) It is never too late to try to retrieve a situation. Of these, invulnerability and macho attitudes are especially hazardous for anaesthetists - and can be compounded by production pressures.
Production Pressure
Other Performance-shaping Factors

There are a number of other performanceshaping factors to be wary of, though there is not sufficient information on these matters to provide a meaningful summary.
Illness and Prescription Drug Use
The degree to which these affect the anaesthetists performance is unknown in the general workplace. All anaesthetists should be registered with a general practitioner and take independent advice when necessary rather than self-medicating.
Alcohol
There have been no studies of anaesthetist performance under the influence of alcohol. However there are some studies equating fatigue and alcohol consumption (see above). It is easy to imagine that performance would be impaired after the ingestion of alcohol, given the known negative effects of alcohol on judgement, motor function and reaction time.
Illicit Drug Use & Drug Addiction
About all that is known for sure is that work performance is one of the last areas of life to become impaired.
There are internal, external, economic and social pressures on the anaesthetist to pursue efficiency and throughput, not safety, as the primary priority. Examples include: Keeping the Theatre Schedule moving speedily, with few cancellations and minimal time between cases; refusing to take breaks and failing to acknowledge the impact of fatigue if the work schedule extends into the evening. When anaesthetists succumb to these pressures they may be prone to skipping appropriate preoperative evaluation & planning, and/or proceeding with elective cases despite medical concerns about the patient doing things that in retrospect they would consider unsafe. If these pressures become internalised they can lead to the development of hazardous attitudes. Production pressure also leads to haste, a precursor to the commission of unsafe acts. In the final analysis, you must ensure that the patients benefit is the primary criterion for your decisions. If you have been pressured to proceed, surgeons or administrators are unlikely to thank you if a patient suffers because of it and may well be disinclined to come to your defence during litigation!
Hazardous Attitudes
It is important to recognise that your attitudes can affect your performance just as strongly as physiologic performance shaping factors. There are five attitudes that are particularly hazardous. 1
1
Note: Hazardous Attitudes (Reference: Aeronautical Decision Making. Advisory Circular Number 60-22. Federal Aviation Administration, Washington, DC, 1991)
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Teamwork Issues: Social Psychology of the Operating Theatre

The operating theatre team has a somewhat ambiguous command structure. The surgeon and anaesthetist are jointly responsible for the patient, with a supporting group of nursing & technical staff. Each has a primary territory of knowledge, skills & responsibility, but there is considerable overlap. The particular individual giving instructions to the rest of the team at any given time will depend on the circumstances. The degree to which various members of the operating theatre team agree on common objectives is also debatable. While all would agree that a good outcome for the patient is the ultimate goal, there can be considerable disagreement on how to achieve this, and which elements of patient care have the highest priority at any given time. The basic social and psychological effects of working in a team should be kept in mind. Team members can be considered in terms of their tasks or goals and their interpersonal or emotional orientation. The democratic style, showing consideration for others, is likely to be appropriate when things are going well. A more autocratic style may predominate if difficulties or emergencies occur. Depending on the circumstances, it may be better to be direct with ones communication, rather than be polite but indirect. Problems arise if an individual is either too demanding or fails to assert proper leadership because of concerns about upsetting colleagues in crises, lowerstatus team-members tend to defer to a higherstatus individual, even if that individual is performing poorly. Role clarity between trainee and supervisor is often not explicit during the conduct of routine anaesthesia this is often compounded during a crisis, because responsibility for different tasks is rarely predefined. It has been demonstrated that interpersonal and communication problems are responsible for many inefficiencies, errors and frustrations in psychologically and organizationally complex environments. Anaesthetists and surgeons that work together on a regular basis tend to be able to sort out problems without a lot of stress. We probably need to place more importance on establishing social relationships in the Operating Theatre 5, 6 . Formal training in team management and
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communication skills can produce substantial improvements in human performance as well as reducing safety-critical errors. Hence the recent trend towards translating Crew Resource Management training in aviation into Crisis Resource Management training in anaesthesia using immersive simulation. While peoples personalities cant be changed, individuals attitudes are relatively malleable to training interventions (see Flin 1 ).
Systems Approach to Patient Safety

(see Reason, 7) Doctors are used to evaluating adverse events in terms of decisions and actions made by individual clinicians. However, it is increasingly recognised that system-wide issues are more important in the prevention of such events. The basic premise of a systems approach is that humans are fallible and that errors are inevitable. Errors originate not from the perversity of human nature but as a result of factors within the system in which we work. When an adverse event occurs, the important issue is not who blundered, but how the systems defences failed. In fact, the term error increasingly is being considered an inappropriate way to categorise behaviours - in that it implies blameworthiness - and should be thought of merely as a way to identify behaviours at the heart of a critical situation see Runciman 8. Countermeasures are based on the assumption that although we cannot change the human condition, we can change the conditions under which humans work. Systems thinking is about two related concepts: Understanding why things happen because of organisational and systemrelated design, procedures, incentives & disincentives. Finding system solutions to problems even if they involve errors by individuals. An example is the patient who goes to ICU after pulmonary aspiration caused by reflux that was noted in pre-assessment clinic, but not by the anaesthetist of record this person had to do a timecompressed, corridor pre-operative assessment. In discussing this case the systems approach asks: How can we change the system to prevent this
happening to others? Rather than just blaming an individual. Key Points of Understanding & Analysis Do not try to assign blame. Most events involve multiple factors. Focus on understanding what occurred and on finding solutions for the future. Dont be satisfied with the easy explanations. Concentrate on the situation as a whole, not on individuals. Assess individual behaviour and performance as a symptom of underlying characteristics of the system. Keep asking why and how questions. For every answer there is probably another why question just around the corner. List deeper causes, even if they are not easily correctable. They put events into perspective and offer targets for long-term change. Look for situations that invite mistakes, or that make it difficult to recover from mistakes. In particular be alert for: Design errors. Lack of, or poorly developed, standard procedures. Reliance on memory or calculation for critical decisions. Areas of conflicting responsibility, such as handover of care, or patient transport. Production pressure. Dont be satisfied with explanations such as Thats the way the system is and theres nothing we can do about it. The system CAN be changed (though it might be tricky and it might take a while!) Recommendations & Solutions Always look for ways to improve the system, regardless of the proximate cause of the particular error or occurrence under review. Look for ways that the system can make up for the inevitable mistakes of individuals. Solutions to problems can include changes in: Training of personnel training only works if it is specific. Design characteristics of equipment or supplies. Positioning of equipment or supplies.
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Operational procedures (e.g. Timeout). Cognitive aids such as checklists. Personnel supervision and staffing levels. As stated previously, many adverse events in medicine result from actions made by persons who know how to perform the relevant task safely, have done so many times in the past and face significant personal consequences for the error. Error is not the monopoly of an unfortunate few, merely the down-side of having a brain! Although we cannot change the aspects of human cognition that cause us to err, we can design systems that reduce error and make them safer for patients.
Summary
Each element of both successful and unsuccessful management of difficult situations has its roots not in the peculiar strengths/weaknesses of the individual practitioner, but rather in the intrinsic nature of the psychology of dynamic decision making under time pressure and stress. An important step in improving patient care is the careful evaluation of the various aspects of human performance that can be improved by changes in training of anaesthetists, by continued education of practitioners, and by alterations in operational systems and policies. However, ultimately, you are responsible for giving the best possible care to your patients. Although perfect performance is unachievable, you should strive to approach it. You must also realise that the real world in which you work may make it difficult to translate your skills into optimal patient care. Experience alone will not guarantee good performance, nor can it make you immune to the types of errors that plague all humans in complex, dynamic domains. Production pressures, distractions and the complexity of cases will challenge your best intentions. An important beginning is to recognise that crises will occur in spite of, or even because of, your best efforts! Therefore try to plan as best you can for the potential disaster waiting to happen that is each next case. Make explicit provisions for failure of elements in the anaesthetic or surgical plans. Prepare yourself to recognise
and manage all the crises that you face, regardless of how they might be triggered. Utilise your departments quality assurance program to adapt your practice as required, based on your own experiences and those of others. As you review cases of your own and others, try to avoid becoming fixated solely on the medical and technical aspects of how a crisis was managed; consider the teamwork aspects and the way in which the larger system helped or hindered patient care. Seek to change those aspects of the situation that impeded optimum management.
GOOD LUCK!
www.chfg.org.uk (accessed May, 2008) - a group founded in the UK by an airline pilot whose wife died as a result of a difficult airway during an emergency caesarean section plenty of interesting articles on error and redesigning systems
References:
1. 2. Flin RH, O'Connor P, Crichton M. Safety at the sharp end. Aldershot: Ashgate; 2008. Gaba DM, Fish KJ, Howard SK. Crisis Management in Anesthesiology. New York: Churchill Livingstone; 1994. Rall M, Gaba D. Chapter 83. Human Performance and Patient Safety. In: Miller's Anesthesia. New York: Elsevier; 2005. Runciman WB, Kluger MT, Morris RW, Paix AD, Watterson LM, Webb RK. Crisis management during anaesthesia: the development of an anaesthetic crisis manual. Qual Saf Health Care 2005;14:1-12. Lingard L, Espin S, Whyte S, et al. Communication failures in the operating room: an observational classification of reccurent typse and effects. Qual Saf Health Care 2004;13:330-4. Lingard L. Perceptions of operating room tension across professions: building generalisable evidence and educational resources. Academic Medicine 2005;80:S759. Reason J. Human error: models and management. BMJ 2000;320:768-70. Runciman W, Merry A, Walton M. Safety and ethics in healthcare: a guide to getting it right. Aldershot: Alshgate; 2007.
3.
4.
Suggested Further Reading:

Cooper JB, Gaba DM. No myth: anesthesia is a model for addressing patient safety. Anesthesiology. 2002 Dec;97(6):1335-7 Designing for Situation Awareness: An approach to user-centred design. Endsley, M.R., Bolte, B., Jones, D.G. (2003) Taylor and Francis, New York - how cognitive engineering can help us understand whats going on in a crisis Kohn LT, Corrigan JM, Donaldson MS. To err is human - building a safer health system: National Academy Press 2000. Tepas, D.I. Paley, M.J. Popkin, S.M. Work Schedules and Sustained Performance. In: Handbook of Human Factors and Ergonomics G. Salvendy (Ed) a comprehensive review of fatigue related studies Weinger, M.B., Englund, C.E. Ergonomic and human factors affecting the anaesthetic vigilance and monitoring performance in the operating room environment Anesthesiol (1990) 73:995-1021. A review of performance modifying factors in anaesthesia Croskerry P, Cosby KS, Schenkel S, Wears R. (Eds.) Patient Safety in Emergency Medicine. 2008; Philadelphia: Lippincott Williams & Wilkins. (due for publication August, 2008) an important general text with the best single discussion of diagnostic error for clinicians Reducing error, Improving safety. British Medical Journal. 320 (7237), 18 Mar 2000. - the entire edition of this journal is useful Human Error in Medicine. Bogner, M.S. (ed.) 1994. Lawrence Erlbaum Assoc., Inc. New Jersey. - especially Chapters 5, 11, 12, 13 Clinical Human Factors Group (UK) 5.
6.
7. 8.
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Cardiovascular Emergencies
CARDIOVASCULAR EMERGENCIES
Assoc Prof Sandy Garden2
This module aims to provide the skills and knowledge to enable the implementation of general and specific therapies for perioperative cardiovascular emergencies. The module excludes the management of children and pregnant women, mechanical cardiovascular support and issues related to invasive monitoring. The most recent recommendations by the American Heart Association and the European Resuscitation Council form the basis of most of the text. It is important to be familiar with the protocols used in the hospital in which you practise, because there are subtle differences between the recommendations of the Australian and New Zealand Resuscitation Councils.
Objectives
To implement general and specific therapies for perioperative cardiovascular emergencies. Upon completion of this module it is expected that the participant will understand how to recognise and provide the perioperative management of the following life threatening cardiovascular emergencies: Myocardial ischaemia & the acute coronary syndromes Cardiac arrest and post-arrest care Peri-arrest conditions and cardiac rhythms Emergency vascular access Hypertensive crises Crises with valvular heart disease Perioperative stroke
Overview
This chapter is a non-exhaustive adjunct to the standard texts and aims to provide a practical guide to cardiovascular crises. The topics have been selected because the greatest perioperative cardiac risk [1] is carried by patients with: Unstable coronary syndromes Unstable or severe angina Recent myocardial infarction Decompensated heart failure Significant arrhythmias (high grade atrioventricular block, symptomatic ventricular arrhythmias in the presence of underlying heart disease, supraventricular arrhythmias with uncontrolled ventricular rate). Severe valvular heart disease
Thank to Drs Paul Dalley and Chris Horrocks for kindly commenting on the draft version of this chapter.
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Supply
Demand Wall tension 3 Heart rate Contractility
Myocardial Ischaemia & Acute Coronary Syndromes

Recommended pre-reading [2, 3]. Coronary artery disease is the leading cause of death in adults in most western countries and in a general medical context it is the most common cause of life threatening arrhythmias and cardiac arrest. In the perioperative context the situation is complicated by the interplay between surgical stress, haemorrhage, coagulation and anaesthesia.
Coronary blood flow Arterial oxygen content
Patients at risk
The revised cardiac risk index identifies patients without active cardiac conditions who are at risk of perioperative cardiac death or non-fatal myocardial infarction [1]: Known coronary artery disease (previous myocardial infarction, previous CABG, or percutaneous intervention). History of congestive heart failure or stroke. Peripheral vascular disease, +/- vascular surgery. Diabetes mellitus Renal Impairment Other risk factors [1, 2]: Smoker Hyperlipidaemia Hypertension Non-sinus rhythm Family history (especially sibling) Age>70 Age<40 and cocaine or metamphetamine abuse Anaemia (Hct<28%) [1]
Left ventricular myocardium is perfused during diastole (dynamic coronary resistance is greatest in systole). Time available for coronary perfusion is inversely related to heart rate. An increase in heart rate increases demand and reduces supply. Perfusion pressure = aortic root diastolic pressure minus left ventricular enddiastolic pressure. Ventricular wall tension is determined by both preload (radius) and afterload (pressure, systemic vascular resistance). Hence a dilated heart has a greater oxygen demand for the same generated pressure. Myocardial ischaemia arises when myocardial oxygen demand exceeds supply. Anaerobic metabolism leads to depletion of ATP, causing systolic and diastolic dysfunction. Local accumulation of anaerobic metabolites may be responsible for pain and arrhythmias.
Management of Acute Myocardial Ischaemia

Identify at risk patients Avoid and treat perioperative events that threaten the myocardial oxygen supply/demand relationship.
Reduced Supply
Reduced Coronary Blood Flow Tachycardia Hypotension Elevated LVEDP Reduced Arterial Oxygen Content Anaemia Hypoxaemia
Increased Demand
Increased Wall Tension Hypertension Hypervolaemia Increased Heart Rate Increased Contractility
Myocardial Oxygen Supply and Demand

In order to understand, identify and manage high-risk situations and events, a clear understanding of the balance between myocardial oxygen supply and demand is critical.
Symptoms in the conscious patient: Chest pain Sweating Reversible ECG changes and haemodynamic perturbations may be noted in anaesthetized patients:
Pressure
3 Wall Tension
Radius
2 Thickness
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ST segment changes of 1-2mm T wave inversion Arrhythmias
Treatment
It is important to make a clear distinction between myocardial ischaemia that is caused by oxygen supply/demand mismatch, and acute coronary syndromes caused by coronary artery thrombotic/occlusive events due to plaque rupture, because the treatment is different. If myocardial ischaemia fails to respond to therapy, it is important to consider the possibility of myocardial infarction. Reperfusion therapy is the standard of care for myocardial infarction in non-surgical patients, but is hazardous peri-operatively because of the concomitant anticoagulation and antiplatelet therapy. In this situation, early discussion with a cardiologist and the surgeon is thus needed to determine treatment and because of the need to consider aborting surgery. Treatment of acute myocardial ischaemia should be tailored to severity of problem: Treat precipitating events and deepen anaesthesia if appropriate. Consider aspirin +/- heparin if acute coronary syndrome is suspected. Consider invasive monitoring and postoperative placement in a high dependency environment. Provide analgesia for chest pain with morphine in awake patients. Reduce myocardial oxygen demand and increase myocardial oxygen supply: Reduce heart rate (cardioselective beta-blocker such esmolol, unless contraindicated by heart failure, cardiogenic shock, conduction block, reactive airways disease). Consider verapamil or diltiazem if asthmatic; or if cocaine induced ischaemia [2]. Normalise blood pressure and ensure adequate coronary perfusion pressure. Aggressively manage hypotension or evidence of end-organ hypoperfusion [2]. Consider the use of a vasopressor or inotrope. Reduce myocardial wall tension nitrates. Consider afterload reduction. Note that nitrates are contraindicated if phosphodiesterase inhibitors such as
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sildenafil (Viagra) taken in previous 24 hours (longer for some analogs). Ensure SpO2 >90% [2], avoid anaemia. Ensure normothermia and avoid shivering. Consider intra-aortic balloon pump in refractory cases [2].
Esmolol
1 cardioselective when infusion rate <300mcg/kg/min. If infusion rate is higher, effect is non-selective. Target Heart Rate = 50-60 [2]. Loading dose 250-500 mcg/kg over 1 minute, then infusion. Infusion dose 25-50 mcg/kg/min increasing by 25-50 mcg/kg/min every 510 min. 9 minute half-life (metabolised by red cell esterase) hence contraindications can be viewed as relative. Contraindications to acute -blockade are bradycardia, AV-block, obstructive airway disease, cardiac failure, hypotension, haemodynamic instability, cocaine induced coronary vasospasm [2].
Nitrates
Predominant action is a reduction in preload (wall tension) due to venodilation, thus reducing myocardial oxygen demand. Avoid in RV infarction because marked hypotension can arise due to the effect of venodilation on RV preload. Sublingual nitroglycerine 0.3 mg. IV nitroglycerine 10 mcg per minute via continuous infusion, increasing by 10 mcg per minute every 3-5 minutes, until response (reduction in symptoms or onset of hypotension) [2]. Systolic BP should not be titrated below 110 mm Hg if previously normotensive, or reduced by more than 25% if hypertensive [2].
Platelet Inhibitors and anti-coagulants

In the perioperative context the use of antiplatelet and anti-coagulant medication requires careful risk-benefit analysis because of the risk of bleeding. Consider proton pump inhibitor if concomitant history of G/I bleeding.
Aspirin
Aspirin 160-325 mg, chewed non-enteric formulation for rapid buccal absorption. A lower dose of Aspirin (75-160 mg) is
acceptable if the risk of bleeding is high [2]. Contraindications: allergy (esp. if asthma), active bleeding (gut, retina), bleeding disorder.
Thienopyridine ADP Receptor antagoninsts (e.g. clopidogrel)

Should be considered especially in patients intolerant of aspirin [2]. Additive effect with aspirin.
Glycoprotein IIb/IIIa inhibitor (e.g. Abciximab)

Interfere with final common pathway for platelet aggregation, but of questionable benefit in the absence of revascularization. Increased risk of major bleeding [2].
Anticoagulants
Low molecular weight heparin (e.g. enoxaparin) or unfractionated heparin should be considered, noting that unfractionated heparin is more readily reversed in the event of haemorrhage.
dissection, increased blood viscosity and increase in oxygen demand. Unstable angina typically presents as rest angina, new-onset angina (<2 months) or increasing angina. The hyperdynamic circulatory state seen in the perioperative period (secondary to tachycardia, fever, anaemia) may predispose to plaque rupture and also increases myocardial oxygen demand, and the postoperative hypercoagulable state predisposes to thrombosis. These syndromes are associated with an increase in the risk of myocardial infarction and death [2]. Patients require monitored care in an environment where facilities and staff for cardioversion or defibrillation are immediately available. The most urgent priority is determining need for immediate reperfusion therapy and exclusion of other potentially lethal conditions such as aortic dissection. Myocardial ischaemia that does not respond to therapy should be re-evaluated and early cardiological referral is needed. The decision to undertake reperfusion therapy is based largely on the 12 lead ECG and the biochemical markers of myocardial cellular damage (Troponin T or I, CK-MB). If there is ST segment elevation that is unresponsive to treatment and/or elevation of biochemical markers, then reperfusion should be considered. The biochemical markers may be normal during the first 6 hours after myocardial infarction. Risk of Death or Non-fatal Myocardial Infarction in Unstable Angina Escalation of symptoms in previous 48 hours Pain >20 minutes, rest pain Clinical evidence of heart failure Age >75 years Angina at rest with ST changes > 0.5 mm New bundle branch block Sustained ventricular tachycardia Troponin T or I > 0.1ng per ml Hypotension Renal impairment Risk of Death Due to Myocardial Infarction Short-term risk of lethal ventricular fibrillation (VF) is maximal in the first 4 hours.
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The Acute Coronary Syndromes [2]

A dynamic continuum including unstable angina/non-ST segment elevation (non-Q wave) myocardial infarction (UA/NSTEMI), and ST segment elevation (Q Wave) myocardial infarction. Unstable angina/NSTEMI is defined by STdepression or prominent T-wave inversion, and or positive biomarkers for tissue necrosis without ST-elevation, and in the appropriate clinical setting (such as chest pain), whereas unstable angina causes no increase in biomarkers of myocardial injury. Typically caused by a reduced coronary perfusion that is secondary to rupture of an atherosclerotic plaque in an epicardial artery. This causes platelet aggregation, thrombus formation and non-occlusive narrowing of the coronary artery. The rupture of the plaque exposes subendothelial collagen and tissue factor, thus enabling platelet aggregation. Other causes include re-stenosis at site of angioplasty or stent, and less common causes include vasculitis, embolus, trauma, coronary artery spasm (e.g. cocaine or methamphetamine induced), aortic
Long term risks related to the infarct size and location. Early diagnosis and reperfusion result in a reduction in infarct size, a reduction in mortality and an improvement in long term ventricular function [3]. Reperfusion therapy involves either thrombolysis, percutaneous intervention (PCI) i.e. angioplasty with or without a stent, or Coronary Artery Bypass Grafting. Thrombolysis is contraindicated after recent surgery because of the risk of bleeding and PCI may be the preferred option, however the need for anticoagulation and antiplatelet therapy renders this choice unattractive. Acute fibrinolysis is of no benefit in the absence of ST elevation (actually increases the risk of myocardial infarction), unless there is true posterior myocardial infarction, or presumed new Left Bundle Branch Block [2]. ST-segment elevation (1mm in 2 continuous ECG leads) is a key indicator for urgent reperfusion [2]. Time from onset of symptoms to reperfusion is critical. Maximal benefit occurs when reperfusion is achieved within 3 hours of occlusion, and current recommendation is re-perfusion (PCI or fibrinolysis) within 90 minutes of first medical contact [3]. If reperfusion is not undertaken there is benefit in treating the acute coronary syndromes with both aspirin and betablockers. They both reduce the risk of myocardial infarction and the risk of death after myocardial infarction. Beta-blockers along with nitrates are first line therapy in angina whereas aspirin has no effect on angina.
Posterior infarction (ST depression in V1V4). Biochemical markers may be normal during first 6 hours. Silent ischaemia more likely in the elderly, in women, those with diabetes or prior heart failure. Isolated Q in lead III may be normal, especially in the absence of repolarization abnormality in inferior leads. Event Management Declare a crisis notify the surgeon. Optimise haemodynamics. Aspirin and beta-blockers should be started early in the absence of contraindications. Urgent consultation with cardiologist, to determine possibility of reperfusion. Differential Diagnoses of Acute Chest Pain or CVS Collapse Aortic Dissection Cardiac tamponade Pulmonary embolus Pneumothorax (Tension) Oesophageal spasm or rupture Pericarditis Pneumonia Cholecystitis
Summary
Patients with reversible ST segment changes or T-wave inversion should be treated as angina. Those with non-reversible ST-segment elevation on the 12-lead ECG should be investigated for possible myocardial infarction and evaluated for reperfusion as soon as feasible (this will usually be after the operation). Patients who have perioperative myocardial ischaemia have higher risk of death in the subsequent 12 months and so need ongoing cardiological follow-up.
Diagnosis of Acute Coronary Syndrome due to Coronary Artery Disease

Typical chest pain unresponsive to nitrates. Transient mitral regurgitant murmur, hypotension, sweating, pulmonary oedema. Twelve Lead ECG changes. ST segment deviation of 0.5mm, or symmetrical precordial T wave inversion 2mm while symptomatic [2]. New onset Left Bundle Branch Block.
Cardiac Arrest & Post-Arrest Care

Objectives
Participants must be able to recognise cardiac arrest, be able to implement the Universal Advanced Cardiac Life Support (ACLS) algorithm and provide post-arrest care.
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Introduction
In 2005, evidence-based changes to the CPR algorithms were accepted by international consensus. Participants should read a summary of these changes [4, 5]. The likelihood of survival and the subsequent quality of life after cardiac arrest are determined by the time taken to restore tissue oxygen delivery with a spontaneous cardiac output. The most recent scientific evidence places increased emphasis on the need for high quality and uninterrupted chest compressions during CPR [4, 5]. This is because effective CPR is required to provide oxygen and metabolic substrates to the myocardium, and this increases the likelihood of restoration of spontaneous circulation. During the first few minutes of a VF cardiac arrest, chest compressions are more important than ventilation. Less ventilation is required because pulmonary blood flow is reduced. Survival after collapse decreases by 7-10% per minute in the absence of bystander CPR, but is 2-3 times better with bystander CPR [6]. During prolonged resuscitation, and during resuscitation for asphyxia (typical cause in children), ventilation should be combined with ventilation. At best, external cardiac massage provides around 30% of normal coronary and cerebral blood flow [7], and it is a temporising measure used while spontaneous circulation is restored. Vasoconstriction may improve coronary and cerebral perfusion pressure during CPR [8]. Three interventions are unequivocally effective in adult cardiac resuscitation Cardiopulmonary Resuscitation (CPR), defibrillation for VF/VT and oxygenation/ventilation. There are important differences between perioperative cardiac arrest, unmonitored in-hospital cardiac arrest and out-ofhospital cardiac arrest. The increased availability of ultrasound in intensive care environments means that in the future, transthoracic ultrasound may become the standard of care for the diagnosis of nonarrhythmic cardiac arrest [9]. The common causes are: Pre-existing cardiac, respiratory or renal disease. Drug-induced problems such as overdose, suxamethonium induced bradycardia, and anaphylaxis caused by any of the chemicals to which the patient is exposed (drugs, chlorhexidine, latex, etc). Error or fault with the anaesthetic technique such as problems with ventilation and oxygenation. Problems with the surgical technique (e.g. vagal stimulation, carbon dioxide insufflation or insertion of femoral prosthesis). Haemorrhage and hypovolaemia Sepsis Embolic phenomena (thrombi, fat, air)
Unmonitored in-hospital cardiac arrest

This is usually caused by unrecognized or inadequately treated progressive physiological deterioration with hypoxia and hypotension. Like perioperative cardiac arrest, the cause must be remedied for resuscitation to be successful, and it is thus important to search for the cause while administering supportive treatment [7].
Out-of-hospital cardiac arrest

This is usually attributed (82% of cases) to VF/VT secondary to heart disease and the treatment is early defibrillation [10]. The likelihood of successful defibrillation falls rapidly with time and the universal advanced cardiac life support algorithm (ACLS) places great emphasis on early defibrillation before the rhythm deteriorates to a non-viable rhythm [6]. Drugs are seen very much as adjuncts to defibrillation. The main role of adrenaline is as an alpha agonist to increase coronary and cerebral perfusion pressures. Meta-analysis of randomised controlled trials comparing adrenaline and vasopressin, showed no difference. Adrenaline remains the drug of choice [7].
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Perioperative cardiac arrest

This is usually attributed to a specific cause which must be remedied for resuscitation to be successful. Hence it is important to search for the cause while administering supportive treatment. It can be difficult to decide when to start chest compressions in a monitored hypotensive patient. In the AIMS data the most common rhythm in perioperative cardiac arrest was bradycardia or asystole.
Recognition of Cardiac Arrest In the anaesthetized patient, cardiac arrest is usually first indicated by the physiological monitors. This should be confirmed by clinical examination [11]. In nonanaesthetised and unmonitored patients, cardiopulmonary resuscitation is recommended if the patient is unconscious, not moving and not breathing. Checking the carotid pulse is an inaccurate method by which to confirm the presence or absence of circulation [10, 12].
30 compressions followed by two breaths (compression rate 100/min, 10 breaths per minute after intubation) [7], venous access and the administration of adrenaline every 3-5 minutes, the identification and treatment of reversible factors. VF/VT requires immediate defibrillation. PEA/Asystole requires immediate thought about causes of cardiac arrest. This is the usual path during anaesthesia. Therapy requires clinical judgment in each situation and the algorithm is only a guide to therapy. The need to exercise judgment is critical in the perioperative context because the cause of cardiac arrest is likely to include reversible factors. It is important to be familiar with the protocols used in the hospital in which you practise because there are subtle differences between the recommendations of the Australian and New Zealand Resuscitation Councils. Leader delegates areas of responsibility In perioperative cardiac arrest there are several skilled individuals in the room or vicinity, and so single or two-person CPR is uncommon. We suggest delegation of the following areas of responsibility: Airway/intubation/ventilation Chest compression - change person doing compressions every 2 minutes [7]. If perfusing rhythm is restored this person can keep a finger on femoral pulse. Monitor and defibrillation IV access and drugs Search for cause i.e. exclude Hs and Ts.
Management of Perioperative Cardiac Arrest [11] Declare a crisis

Notify the surgeon/stop surgery and pack wound. Call for help and a defibrillator. Place patient supine and expose the chest. Discontinue anaesthetic agents (infusions and vaporisers). Administer 100% oxygen and verify gas composition. Institute CPR (Basic Life Support) Push hard, push fast, allow full chest recoil, minimize interruptions in compressions, and defibrillate promptly when appropriate [4]. Undertake rapid and complete systematic assessment of the patient, the equipment and drugs, even if the cause is thought to be identified. Common errors are failure to discontinue anaesthetic agents and failure to administer 100 % oxygen check these when you go to help someone else manage a crisis.
Universal ACLS Algorithm

See Figure 1. The Universal ACLS Algorithm as approved by the International Liaison Committee on Resuscitation (ILCOR) [7] has only two possible treatment pathways based upon the cardiac rhythm. One path is for patients with shockable rhythms (Ventricular Fibrillation (VF) or pulseless Ventricular Tachycardia (VT)), and the other path is for patients with nonshockable rhythms (Pulseless Electrical Activity (PEA) or Asystole). The remainder of the algorithm is identical: chest compression, airway management and ventilation with a compression to ventilation ration of 30:2, i.e.
21
Hunt for Ventricular Fibrillation or Ventricular Tachycardia

In out-of hospital cardiac arrest, the most common rhythm at the time of arrest is VF, preceded by either VT or SVT [7], and immediate defibrillation should be undertaken with the following caveats: Interruptions to external cardiac massage should be minimized. CPR should be resumed immediately after each shock, and should continue for 2 minutes before rhythm or pulse are assessed. After successful defibrillation the restoration of effective cardiac output
typically takes a few minutes, and CPR should be continued during this time. The earlier recommendation of three stacked shocks no longer applies. This change is based on efforts to reduce interruptions to chest compression, and evidence that modern biphasic defibrillators have a 90% first shock efficacy. If the delay between collapse and CPR is >5 minutes, then 2 minutes of CPR should precede defibrillation. This increases the likelihood of restoring a perfusing rhythm after shock delivery [6, 7]. Risks to healthcare workers are shock, and spark fire in oxygen enriched environment. Do not charge defibrillator until after all clear command. Modern defibrillators take less than 5 seconds to fully charge. Biphasic defibrillator first shock 120200J, based on the manufacturers recommendations. If the manufacturers recommendation is unknown, then use 200J [6]. Monophasic first shock 360J. Precordial thump may be of use in first 10 seconds after witnessed VF onset. Drugs are adjuncts to defibrillation. There is no evidence of efficacy of drug therapy in improving long-term survival. The new recommendations deemphasize the role of drug administration and reemphasize basic life support [4]. Adrenaline 1mg every three to five minutes. If a perfusing rhythm is transiently restored, but cannot be maintained (recurrent VT/VF), consider early administration of antiarrhythmic medication. For children, 4J/kg, irrespective of energy waveform [6]. If the initial rhythm is not VF/VT, then immediately search for a cause do not assume a myocardial ischaemic aetiology. The recent increase in availability of ultrasound in intensive care environments means that in the future, transthoracic ultrasound may become the standard of care for the diagnosis of non-arrhythmic cardiac arrest [9].
Hypo/or/hyperkalaemia; hypomagnesaemia; hypercalcaemia Hypo/or/hyperthermia Tension pneumothorax Tamponade (trauma, renal failure, thoracic malignancy) Thromboembolus/ pulmonary embolus Toxicity (including anaphylaxis and overdoses tricyclics, -blockers, Ca++ channel blockers) Echocardiography can be considered in the presence of life-threatening cardiovascular instability where the diagnosis is unclear or the response to initial therapy is inadequate. Pulseless Electrical Activity (PEA) and Asytole [7, 8] Although PEA and Asystole are grouped together in terms of their causes and treatment, this can be somewhat misleading because of important differences in outcome. PEA is cardiac electrical activity in the absence of palpable pulse. There are often weak contractions that can be detected with invasive monitoring or echocardiography. It is often caused by reversible conditions that must be sought and treated. If the initial rhythm is PEA then there is a far greater chance that there is a treatable underlying cause for the cardiac arrest. There is a heterogeneous group of rhythms Rapid attention to differential diagnosis Treatment is CPR and adrenaline Asystole: Survival rate from a cardiac arrest with asystole is dismal [8]. Resuscitation is dependent upon identifying and treating the cause. Treatment is adrenaline and atropine (3mg as a single bolus). Rapid attention to differential diagnosis. Pacing for asystole does not improve outcome except: - In complete heart block, so examine ECG carefully for presence of P waves [7]. - After cardiac surgery where pacing may be effective [13]. Defibrillation for asystole or fine VF increases myocardial injury and is not recommended [7].:
Search for cause (memorize 4 Hs and 4 Ts)

Hypovolaemia (the most common cause) Hypoxaemia
22
Figure 1. Universal Advanced Cardiac Life Support Algorithm [7]. NB. It is important to be familiar with the protocols used in the hospital in which you practise. There are subtle differences between the recommendations of the Australian and New Zealand Resuscitation Councils.
23
Post Resuscitation Care and Periarrest Conditions [7, 14]

The immediate goals of post-resuscitation care are to: Optimise cardiopulmonary function and systemic perfusion, especially to the brain. Identify precipitating causes. Institute measures to prevent recurrence. Institute measures that may improve longterm, neurologically intact survival. Global Review Repeated re-evaluation should be undertaken. Hypoxia, hypercarbia and hypotension all increase the risk of further cardiac arrest, and contribute to secondary brain injury. Postarrest patients will frequently have haemodynamic instability with: Bradycardia or tachycardia. Myocardial depression/stunning with systolic and diastolic dysfunction. Cerebral dysfunction and loss of cerebral autoregulation. This will result in pressure dependent cerebral blood flow, and so hypotension should be aggressively treated. Seizures occur in 5-15%. Patients may sustain fractured ribs and pneumothorax from compressions. These are the leading causes of postresuscitation mortality and should be treated aggressively. ABCD problems are a common cause of post-resuscitation hypotension and arrhythmia. Secondary Survey Airway Ventilation R=L Breathing SpO2, paralyse, sedate Circulation IV access, monitoring (vital signs, urine output, invasive monitoring). Verify placement of all catheters and cannulae Diagnose Cause 12 lead ECG, electrolytes, & Complications (Na+,K+,Ca++,Mg++,blo od gases), drug screen, glucose CXR (#ribs, pneumothorax, tracheal tube), consider tamponade.
The severity of myocardial dysfunction in the post-resuscitation period is related to the duration of global myocardial ischaemia. Inotropes or vasopressors may be needed to treat the hypotension from systolic dysfunction. Volume loading may be needed to optimise preload in context of impaired diastolic relaxation. The patient may be hypoxaemic secondary to gross V/Q mismatching and should be ventilated with 100% oxygen until the oxygenation is stable. Early neurologic assessment is an unreliable indicator of ultimate recovery of cerebral function, assessment at 72 hours is more reliable. Up to 20% of initially comatose survivors of cardiac arrest may have good 1year neurologic outcome [14]. Hyperventilation may worsen neurologic outcome, and normocarbia is recommended. Mild induced hypothermia (32-34C) improves neurologic outcome among initially comatose survivors, but its practical application may be difficult. Patients should not be rewarmed from mild spontaneous hypothermia (>33C), and hyperthermia should be avoided because it increases cerebral metabolic rate and is associated with a worse neurologic outcome [14]. Tight glycaemic control is recommended. Hypotension The specific causes must be sought and treated. The causes of hypotension and cardiac arrest during anaesthesia are different from and additional to causes in other settings. In the AIMS study the most common causes of hypotension were drugs, regional anesthesia and hypovolaemia. There may be more than one cause for example, hypovolaemia and neuraxial blockade [15]. Supportive therapy: Volume administration Inotropic support
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Life Threatening Cardiac Rhythms [7]

See figure 2. The aim of this section is to provide an initial approach to the patient who has a life-threatening cardiac arrhythmia. The management of patients with cardiac arrhythmias is driven by clinical assessment and the need to make timely decisions: Is the situation immediately threatening? Does the patient need CPR? Is the rhythm slow or fast?
Urgency Life threatening Rhythm Bradycardia
Disorders of impulse conduction - blocked or re-entrant. Combinations of these.
Management of Cardiac Arrhythmias

See table 1 and Figure 2. There are three basic questions: What is the rhythm? There are two basic possibilities - Bradycardia and Tachycardia. When looking at the ECG address the following points. Is there a P-wave, if so what is its relationship to the QRS? Is the QRS morphology normal, what is it width, and is the rhythm regular? What is the underlying cause [16, 17]? Perioperative arrhythmias generally occur in patients who have structural heart disease and some sort of factor that initiates the arrhythmia. Acute ischaemia Sympathetic
life
Initial Therapy Most readily available of Electrical therapy - Pacing Drugs
Tachycardia Unstable but not immediately life threatening Tachycardia Bradycardia
Electrical therapy - Cardioversion Reverse cause Consider drugs Reverse cause Consider drugs
Table 1. Simplified Approach to Dysrhythmias
If the patient is unstable with serious signs or symptoms, then urgent and invasive therapy is indicated. Serious signs and symptoms include hypotension (SBP<90 in a conscious patient, a lower pressure is usually tolerated in anaesthetised patients), heart rate >150 or <40, reduced level of consciousness, chest pain, congestive heart failure.
stimulation Drug effects Electrolyte imbalance (especially hypokalaemia and hypomagnesaemia [1]). Hypoxia, hypercarbia What is the treatment? This is determined by the clinical urgency and the availability of equipment (e.g. pacemaker for bradycardia). Always address the contributory factors as well as the arrhythmia.
Bradycardia
Most perioperative arrhythmias are caused by remedial non-cardiac causes such as infection, hypotension, medications, metabolic derangements and hypoxia [1]. These should be sought and treated. Patients with serious arrhythmias should have IV access and oxygen therapy. Preoperative evaluation of a patients ECG may identify predisposing features. Mechanisms of Cardiac Arrhythmia Disorders of impulse generation increased or decreased.
Bradycardia may be absolute (e.g.<40 beats per
minute) or relative (inappropriately low in the physiological context). The treatment for symptomatic bradycardia, irrespective of cause [7], includes stopping vagal stimulation and then the critical decision is whether to pace or to use drugs. Initial drug therapy is atropine 500mcg repeated to a total of 3 mg. If initial response is satisfactory, re-evaluate to consider risk of asystole. The risk of asystole is higher if: recent asystole, Mobitz
25
II AV block, complete heart block with wide QRS, or ventricular pauses >3 seconds. In absence of response to atropine, adrenaline is the recommended second line medication [7]. Third-line drug therapies include aminophylline, isoprenaline, dopamine, glucagon (if -blocker or Ca++-blocker overdose) and glycopyrollate. Unstable symptomatic patients should have transcutaneous cardiac pacing, atropine and/or adrenaline, as a bridge to transvenous pacemaker. Pacing should be available for stable patients where there is a perceived risk of asystole. Perioperative bradyarrhythmias are usually caused by medications, electrolyte disturbances, hypoxaemia or ischaemia [1]. Supportive therapy should be concurrent with identification of, and therapy for, underlying causes. Sinus bradycardia, First Degree Block & Second Degree Block Mobitz Type I Rarely symptomatic. All of these may be caused by excessive vagal stimulation, especially if patient receiving digoxin, -blocker, verapamil. Second Degree Block has intermittent failure of A-V Conduction. Mobitz Type I block is generally benign and asymptomatic. Block is usually at A-V node, with a normal His-Purkinje System. There is a progressive increase in delay between P and QRS, until a QRS complex is missed, causing an irregular QRS rhythm. Sick Sinus Syndrome Alternating bradycardia and tachycardia. Treatment combination of antiarrhythmics and permanent pacemaker. Second Degree Block Mobitz Type II More ominous than Mobitz Type I. Intermittent failure of AV conduction with loss of QRS complex; without progressive increase in delay between P and QRS. Irregular QRS rhythm. Usually caused by myocardial infarction or chronic degeneration of conduction system.
May progress unexpectedly to third degree heart block. Symptomatic patients should be referred to a cardiologist for permanent pacing. Third Degree Block Total failure of A-V conduction. Block is usually below A-V node and involves total block through both bundles, hence wide QRS. Regular QRS rhythm. This is an unstable rhythm that is associated with extreme bradycardia and episodes of ventricular asystole. Usually caused by myocardial infarction or chronic degeneration of conduction system. Emergency Pacing [7, 18, 19] Indications Haemodynamically unstable bradycardia (SBP<90, altered mental state, angina, pulmonary oedema). Especially if unresponsive to drug therapy. Bradycardia with pause dependent ventricular rhythm (risk of ventricular tachycardia or ventricular fibrillation). Cardiac arrest secondary to drug overdose, acidosis, electrolyte disturbance or other reversible process. After cardiac surgery. Relative Contraindications Severe hypothermia (risk of triggering VF and VF, these are also more difficult to treat) Brady-asystolic arrest >20 minutes (patient is already dead). Technique for Transcutaneous Cardiac Pacing This is the first choice in emergency cardiac care. Modern defibrillators should have transcutaneous cardiac pacing capability. Recommended output is more or less twice the output of a standard peripheral nerve stimulator and there is no significant bystander risk (in contrast to cardioversion/defibrillation). Apply large diameter (8cm) stick-on electrodes. The anterior electrode is placed to the left of sternum at the cardiac apex. The posterior electrode is placed
26
immediately behind the anterior electrode, to the left of the spine. Initiate pacing. Default rate is typically 80 per minute. Select either fixed rate or demand pacing. Gradually increase the output until capture is achieved (most transcutaneous cardiac pacing systems have an output current of 0-200 m Amps). Pace at 10% above capture threshold. Check that the pacing current is triggering the ventricle to depolarise. You should see a wide QRS complex and a broad T wave. Ensure mechanical capture, i.e. pulse synchronous with ECG. Complications of Transcutaneous Pacing The pacemaker current has a duration of 20 - 40 milliseconds and this current may conceal the underlying rhythm. This may cause the operator to fail to recognise either non-capture or underlying ventricular fibrillation. A special blanking facility that conceals the pacemaker current must be incorporated in the equipment. Pain from electrical stimulation of skin or muscle may make this difficult in the conscious patient, hence analgesia and sedation are required. Tissue damage with prolonged use. Fist Pacing If atropine is ineffective, fist pacing may be used while awaiting transcutaneous pacing. Serial rhythmic blows to the lower edge of the sternum with a closed fist.
Tachyarrhythmias [7, 17, 19]

As a rule of thumb, broad-complex tachycardia is tolerated less well than narrow complex tachycardia, and most wide complex tachycardias are ventricular in origin. Atrial fibrillation (AF) is the most common sustained arrhythmia encountered. Irregular rhythms are usually atrial fibrillation. Because of the risk of thromboembolus, patients should not be cardioverted without prior anticoagulation or TOE exclusion of atrial thrombi, unless the duration of atrial fibrillation is less than 2 days [20, 21]. In patients with no adverse signs and duration of AF more
27
than 2 days, the immediate goal is rate control, with consideration of anticoagulation and delayed cardioversion. Ventricular rate control in atrial fibrillation is most effective with beta blockers, followed by calcium channel blockers, and lastly digoxin [1]. Target rate is 60-80 at rest or 90-115 with moderate exercise [20]. In patients with AF of >48 hrs (or unknown duration) and requiring immediate cardioversion, concurrent anticoagulation with heparin is indicated because of atrial hypokinesia and risk of thrombus formation after cardioversion [20]. This applies to synchronised DC shock and pharmacological conversion (flecainide or amiodarone) [22]. There is a clustering of stroke risk at the time of onset of AF [23]. Tachyarrhythmias are usually differentiated on the basis of site of origin (supraventricular or ventricular). This distinction is important because ventricular tachycardia may degenerate into VF, whereas SVT is less hazardous. In addition the pharmacological treatments are different. Most patients with wide-complex tachycardia will have VT and should be treated as such in first instance, even though some will have SVT with Bundle Branch Block. Most patients with narrow-complex tachycardia can be assumed to have supraventricular tachycardia. Both VT and SVT reduce the diastolic period and thus may reduce myocardial perfusion and precipitate myocardial ischaemia. A cardiology opinion should be sought, although emergency treatment should not be delayed. It can be difficult to decide if the tachycardia is due to hypotension or the cause of hypotension. Contributory factors should be sought and corrected. Failure to do so reduces the likelihood of sustained cardioversion High circulating catecholamines. Hypokalaemia (if K<3.6 give K at rate of 20 mmol per hour) and then check it. Hypomagnesaemia (assume low if K low, give 8 mmol (4 ml 50%) slowly over 1-2 minutes), and repeat if necessary.
Table 2. Simplified antiarrhythmic choices
Treatment Haemodynamically unstable patients with sustained supraventricular or ventricular tachyarrhythmias should be cardioverted. The shock should be synchronised with the R wave to minimize the risk of inducing ventricular fibrillation. Contributory factors should be corrected in all patients (e.g. treat hypomagnesaemia in torsades de pointes). Antiarrhythmic drug therapy is indicated if the patient is haemodynamically stable, or has failed cardioversion; or to facilitate rhythm stabilisation after successful cardioversion or defibrillation. Vagal stimuli will terminate about 25% of episodes of paroxysmal SVT (ask patient to blow plunger up 20 ml syringe) [7]. Synchronised Cardioversion Cardioversion implies a synchronised shock as opposed to the unsynchronised shock of defibrillation. Indications: Preferred over antiarrhythmics if serious sign or symptoms, HR>150, failed drug therapy. Broad complex tachycardia and atrial fibrillation require large energy shock: Monophasic 200J or biphasic 120150J Atrial flutter and supraventricular tachycardia require lower energy: Monophasic 100J or biphasic 70-120J Pulseless VT treated as VF (asynchronous defibrillation). Antiarrhythmics [17] Drug therapy is based on the proposed mechanism of arrhythmias: Increased automaticity, triggered activity or re-entry in the conduction system. Every drug that is administered unsuccessfully will add to myocardial depression and can be proarrhythmic (a classic example is quinidine causing torsades de pointes).
Wide-Complex Tachycardia Amiodarone Narrow-Complex Tachycardia Adenosine for SVT Atrial Fibrillation Esmolol for rate Amiodarone or Flecainide for rhythm Ca++-blocker, amiodarone digoxin for rate
Amiodarone [7] Effective in a broad range of supraventricular and ventricular tachyarrhthmias. Predominant action is Class III antiarrhythmic. Prolongs action potential duration and the refractory period of all cardiac cells by blocking repolarising K+ current, thus inhibiting reentry. Amiodarone also blocks sodium channels, -receptors and calcium channels. Vasodilatation ( -blockade, Ca++ blockade, and direct histamine release by diluent) may cause hypotension, but cardiac output generally preserved. In unstable patients, if VF/VT persist after three shocks administer 300mg amiodarone as a bolus, a further 150 mg may be given for recurrent or refractor VF/VT. In stable patients, with VT or SVT, administer 300mg amiodarone over 20-60 minutes. Additional infusions of 150 mg. Lignocaine [7] Class 1b antiarrhythmic. Suppresses ventricular arrhythmias by decreasing the slope of phase 4 depolarisation (thus reducing automaticity) and by reducing slope of phase 0 rapid depolarisation (thus slowing conduction through ischaemic areas). It acts preferentially on ischaemic tissue and blocks fast sodium channels. At the usual concentration it has no significant effect at atrial, SA or AV node tissue. Lignocaine causes less reduction in myocardial contractility than amiodarone. When used in conjunction with other antiarrhythmic agents lignocaine may cause a reduction in contractility and blood pressure. Recommended for VF/VT only if amiodarone is unavailable, should not use both Initial intravenous dose 1-1.5 mg per kg Infusion 15-50 mcg per kg per minute Magnesium [7] 8mmol magnesium is recommended for refractory VF and VT if there is suspicion of hypomagnesaemia, e.g. K+ losing diuretics. Can be given for ventricular rate control in atrial fibrillation [7] Also indicated for torsades de pointes and digoxin toxicity Bicarbonate Only recommended if cardiac arrest associated
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First Choice
Second Choice
Lignocaine
Amiodarone Esmolol Digoxin
or
with hyperkalaemia or tricyclic antidepressant poisoning. Administer 50mmol [7] Adenosine Acts via adenosine receptors on the cell surface to reduce automaticity and slow conduction at AV node. It activates potassium channels and hyperpolarises the cells. Inhibits adenylate cyclase and thus reduces intracellular cAMP, leading to inhibition of inward Ca++ and pacemaker currents. The effect is limited to SA and AV nodes, thus causing a reduction in SA node rate and a decrease in AV node conduction, thus interrupting re-entrant pathways. It has little effect on atrial tissue, accessory pathways, His-Purkinje or Ventricular cells (they lack the adenosine responsive K+ channel). Used primarily to terminate paroxysmal supraventricular tachycardia by blocking reentrant pathways. Paroxysmal SVT has different mechanisms, with 90% due to AV nodal re-entry (60%), or AV re-entry mediated by an accessory pathway (30%) [24]. Adenosine is indicated for both, with the proviso that in AV re-entrant tachycardia, e.g. Wolff-Parkinson-White syndrome conduction across the accessory pathway may be facilitated and may precipitate a rapid ventricular response. In non-re-entrant arrhythmias (e.g. a-flutter and atrial tachycardia) adenosine may cause transient AV block and slowing of the heart rate, allowing the atrial rhythm to be detected visually, thus enabling a diagnosis to be made. Because of transient vasodilatation and hypotension it is no longer recommended as a method to allow VT and SVT to be differentiated. [17]. Xanthenes competitively inhibit adenosine receptors, therefore may need to increase the dose of adenosine if the patient takes caffeine or theophylline. May need less if concurrent carbamazepine. Adenosine has half-life of 10-15 seconds due to rapid sequestration by red cells. This is important because it means that it needs to be administered as a rapid bolus and its effects are short-lived, including side-effects (headache, chest pain, flushing, and bronchoconstriction).
Initial rapid bolus 6mg followed by 20 ml saline flush. Brief asystole up to 15 seconds is common. If no response in 2 minutes, then administer 12 mg. Failure to terminate a narrow complex tachycardia with adenosine or vagal manoeuvres, suggests an atrial tachycardia such as atrial flutter [7]. Esmolol See section on myocardial ischaemia. Verapamil Although verapamil is very effective in narrow complex tachycardia, it can be extremely dangerous. For example, like adenosine, it can increase the ventricular rate in patients with Wolff-Parkinson-White syndrome. It is not an early choice for most anaesthetists because it can reduce myocardial contractility in patients with depressed ventricular function, and can cause gross bradycardia in patients treated with -blockers or inhalational anaesthetics.
Cardioverter/Defibrillators [25]
A defibrillator is a device that delivers a controlled electric shock to terminate a cardiac arrhythmia. This requires the passage of a sufficient current through the heart to depolarise all myocardial cells simultaneously, with the expectation that normal electrical activity will resume. Cardioversion is the same principle, but with the use of a synchronised shock applied to a rhythm other than VF. Cardioversion requires less energy and 100J is the most common initial energy, except for atrial fibrillation where a larger initial shock (200J) is recommended [20]. A variety of automated devices are now available. Defibrillator Features and Operation A capacitor that stores the current Control switches to allow charging and discharging by the operator Controls that allow the operator to select a delivered energy level (Joules) A choice between a synchronised or nonsynchronised shock. Unsynchronized mode is usually the default setting.
29
Current
Energy (R=resistance and t=time) R.t
Modern defibrillators deliver their energy as a biphasic waveform. They have a greater first-shock efficacy for long duration VF/VT than monophasic defibrillators, and do so with lower delivered energy. Monophasic defibrillators although widely used are no longer manufactured. Biphasic energy recommendations are manufacturerspecific. This is because the required energy varies depending upon the specific waveform of discharge. Optimise transthoracic resistance Good contact with chest wall Appropriate size of electrode (large) and use of conductive gel End-expiratory timing (air in the chest increases the impedance) Bone is a poor conductor and should be avoided Electrode placement Aim is to maximise current flow through the heart Anterior electrode right parasternal, below the right clavicle Apical electrode is midaxillary line at level of nipple Synchronisation Used to avoid the risk of inducing VF. The shock is synchronised relative to QRS, so that the shock is delivered after the relative refractory period Many defibrillators re-set to the asynchronous mode after delivering a shock and need to be re-set to the synchronised mode If there is a delay in synchronisation (for example a problem sensing the QRS complex) then use an unsynchronised shock Hazards to patient Damage to heart - choose the minimum effective energy. Initial shock energy reflects a compromise between probability of success and risk of harm
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The shock energy should be increased only if a shock fails to terminate the rhythm. If the defibrillation is effective but the arrhythmia recurs, then the problem is recurrence, not failure to defibrillate and so re-shock with the same energy. Address the underlying cause and add an antiarrhythmic drug. Be sure to differentiate failure to defibrillate from rapid reversion to VF. Electrical induction of VF may occur with asynchronous shocks Insufficient or wrong gel, including metallic GTN patches can cause arcing and burns or fire risk Damage to implanted pacemakers or defibrillators - try and avoid defibrillation directly over implanted devices Hazards to healthcare workers Give clear warning of impending shock. Do not charge defibrillator until after all clear. Modern defibrillators require less than 5 seconds to charge. Procedure for Defibrillation It is essential to be familiar with the equipment used in your own hospital. Defibrillation/cardioversion will be practiced at a skill station.
Wide-Complex or Atrial Fibrillation 120-150 J 200 J Narrow-Complex or Atrial Flutter 70-120 J 100 J
Biphasic Monophasic
Table 3. Simplified first shock energy settings [6]
Figure 2. Universal algorithm for tachycardia with pulse [7]. NB. It is important to be familiar with the protocols used in the hospital in which you practise. There are subtle differences between the recommendations of the Australian and New Zealand Resuscitation Councils.
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Crises with Valvular Heart Disease

Pre-reading from an authoritative book on cardiac anaesthesia such as Chapter 20 in Kaplan [26] is recommended. The management of crises in patients with valvular heart disease is significantly aided by the correct diagnosis. In broad terms the risk of a perioperative cardiac event is greatest with a stenotic lesion than a regurgitant lesion, and aortic stenosis is the most common. Diagnosis is crucial because the therapy for stenotic lesions may include a reduction in heart rate and an increase in afterload, whereas the converse is typically advocated in regurgitation. With aortic stenosis there is an increased perioperative risk is myocardial ischaemia, and with mitral valve disease there is an increased risk of heart failure and atrial dysrrhythmias. [1].
myocardial ischaemia without having coronary artery disease.
Aortic Regurgitation
Tachycardia useful to optimize forward flow. A critically low diastolic pressure in the presence of a high left ventricular diastolic pressure may compromise coronary perfusion, and in the event of cardiac arrest, coronary flow will be particularly poor during CPR.
Mitral Valve Disease

Patients with symptomatic mitral stenosis or regurgitation carry an increased risk of perioperative congestive heart failure [1]. Mitral valve disease is associated with pulmonary hypertension and atrial arrhythmias (especially atrial fibrillation). Tachycardia is poorly tolerated in severe mitral stenosis because of limited time for atrial emptying (and thus left atrial pressure rises further, and left ventricular filling is compromised). In contrast after-load reduction is helpful in mitral regurgitation.
Aortic stenosis
Aortic stenosis is the most common valvular heart disease in the elderly, affecting between 2 and 9 percent of adults over the age of 65 and is concomitant with coronary artery disease in 50% of patients [27]. Severe aortic stenosis (mean pressure gradient > 50mm Hg, valve area < 1 cm2 or symptomatic) poses a high risk of perioperative myocardial infarction and symptomatic patients should be offered valve replacement prior to elective non-cardiac surgery [1]. Risk is also related to the extent of left ventricular hypertrophy, the presence or absence of left ventricular dysfunction and the type of surgery. The rate of complications is much higher in patients with undiagnosed severe aortic stenosis [27]. Because of reduced ventricular compliance, a high filling pressure is required and maintenance of preload is desirable. Sinus tachycardia or atrial arrhythmias can worsen the load on the left ventricle, causing heart failure and/or myocardial ischaemia, and blockade should be considered, aiming for a heart rate of 50-60. Hypotension may cause a dramatic reduction in coronary perfusion and should be treated aggressively with an agonist. Patients with aortic stenosis or hypertrophic cardiomyopathy may develop
32
Hypertrophic cardiomyopathy [28]

This disease is more common than previously recognized (1:500) and is frequently undiagnosed. Dynamic left ventricular outflow tract (LVOT) obstruction due to asymmetric septal hypertrophy is particularly relevant to perioperative care. The outflow tract obstruction is worse with increases in contractility, reduction in preload, or a decrease in ventricular volume. Vasodilators will worsen the LVOT obstruction and any associated mitral regurgitation. Histologic features include disorganised cardiac muscle cell architecture (found in 95% of patients who die of this disease, and not confined to hypertrophic regions), reduced density of arterioles relative to degree of hypertrophy, myocardial fibrosis. Symptomatic patients fall into three main groups: progressive heart failure (+/- angina), atrial fibrillation, or sudden death due to arrhythmias. Paroxysmal atrial fibrillation is poorly tolerated because of the diastolic dysfunction and may cause acute deterioration. For patients at high risk of sudden death, an implanted cardioverter-defibrillator is the current treatment of choice.
These symptom patterns are the typical cause of perioperative cardiac morbidity and mortality, and as with valvular heart disease, unrecognized lesions are a significant problem. For example a patient who sustains acute haemorrhage resulting in systemic hypotension, will develop dynamic LV outflow obstruction and the situation may be aggravated by the administration of adrenaline. Strong consideration should be made for perioperative -blockade.
administered. Caution should be exercised if administering -blockers without vasodilators in this context, because of the risk of precipitating acute left ventricular failure. Subsequent investigation should be considered to exclude rare and unexpected conditions such as thyroid storm, phaeochromocytoma, and other endocrine causes of hypertension [31].
Perioperative Stroke [32, 33]

Perioperative stroke is rare outside the context of cardiac or vascular surgery. Emergency neurologic consultation is required. Nearly 2/3 of cases are embolic in origin and treatment options are limited because systemic Tissue Plasminogen Activator (t-PA) is likely to be contraindicated because of the risk of haemorrhage at the surgical site. Outside the perioperative context, fibrinolytic therapy for stroke results in improved outcome. Fibrinolysis must be administered within three hours of onset of symptoms, and so is administered to less than 10% of stroke patients. Perioperative therapeutic options all require interventional radiological procedures and include intraarterial thrombolysis, mechanical thrombectomy or embolectomy. All of these require intervention within 6 hours of stroke onset, and so rapid diagnosis and treatment are required. Diagnostic investigations should include a CT scan of the brain to exclude haemorrhage; and a 12 lead ECG to exclude atrial fibrillation or recent myocardial infarction as sources of embolic stroke. Supportive measures include those directed at reducing secondary injury, such as avoiding hypoxaemia, hypotension, fever, and ensuring tight glycaemic control.
Hypertensive Crises [29]

The perioperative risk attributed to hypertension is related to the extent of hypertension-induced
end-organ damage rather than the blood pressure per se. However, patients who have poorly treated severe hypertension (e.g. 180209/110-119) have an increased risk of intraoperative cardiovascular lability and perioperative myocardial ischaemia. Therapy for perioperative hypertensive crises should be directed at the underlying cause of the acute hypertension and the related morbidity. The most common causes of severe intraoperative hypertension identified in the first 4000 AIMS reports were the inadvertent administration of a vasopressor (40%), excessive surgical stimulation or light anaesthesia (21%), and failure to deliver the anaesthetic (14%). Other less common causes included hypercapnoea, pre-eclampsia, carcinoid syndrome, and phaeochromocytoma. Serious morbidity occurred in six patients and consisted of myocardial infarction, pulmonary oedema and awareness [30]. Immediate treatment [31]: Stop the surgery until control is achieved. Exclude measurement error (repeat the measurement, correct cuff size, ensure the transducer has not fallen to the floor). Treat the cause (e.g. deepen the anaesthesia with 10-20 g/kg alfentanil, check that the ventilation and oxygenation are adequate, check that this is not the response to intracranial hypertension in head injured patients. Consider uncommon problems such as malignant hyperthermia or autonomic hyper-reflexia if chronic spinal cord injury). Consider specific antihypertensive therapy such as vasodilators and beta blockers. Check that usual antihypertensives has been
33
Emergency Vascular Access

The traditional EMST/ATLS approach has been to undertake two attempts at peripheral venous cannulation, and failing that to undertake peripheral venous cut-down. The use of venous cut-down is now controversial because the complication rates of cut-down are similar to femoral vein cannulation and central
vein cannulation (although the complications here are more serious). Cut-down takes longer to achieve, the complication rate is mostly related to operator experience and it is probably more appropriate to limit their use to surgical personnel. In trauma patients, consider caval injury, and have IV access above or below diaphragm, depending on site of injury. Cervical injury is a relative contraindication to internal jugular. With chest injury, place the central line on same side as chest injury to avoid injury to good lung. Poisseulles law determines flow rate. If using vascular sheath with a side arm as a volume line, ensure that any valves are capped, to avoid air entrainment with rapid infusion. It has been recommended that in any evolving crisis, that the satisfactory placement of existing vascular access should be questioned [34]. Extravasated lines used with pressure infusion systems can cause a compartment syndrome.
Vascular Access Options

Peripheral vein Percutaneous - procedure of choice. Cut-down requires surgical expertise long saphenous, cephalic, basilic, median cubital. Central vein When peripheral sites not available. Low complication rate with experienced personnel. Life threatening complications include haematoma, haemo/pneumothorax, hydrothorax, cardiac tamponade, air embolus, and arrhythmia. Complication rate increases with each needle pass and success is very unlikely after 5 needle passes. Consider ultrasound-guided access. Femoral vein Cannulation has less immediate complications and can be undertaken concurrently with airway management. Intraosseous [8] The device must be flushed before use, and a lignocaine bolus (2ml of 2% lignocaine)
34
is recommended to reduce pain with infusion. Other than stating that resuscitation drugs can be administered by this route, ILCOR has not specifically stated which drugs can be administered. In a dog model, the Intraosseous is similar to intravenous in terms of pharmacokinetics and dynamics for adrenaline, sodium bicarbonate, calcium chloride, hydroxyethyl starch, 50% dextrose in water, and lignocaine . Can be used in all age groups. Typically used most successfully in preschool children (less than 6 years), because the cortical bone is softer and intramedullary flow rates are higher. http://www.facs.org/trauma/publications/v asaccess.pdf However, specific equipment is now commercially available for use in adults. Intraosseous route is accepted by the European Resuscitation Council and the American Heart Association as an alternative form of IV access in adults. [7, 35, 36]. When modern access devices (e.g. power drill) are used, access is safer and faster than central venous access, with a typical insertion time of 10 seconds. Pharmacokinetics are similar to central venous access and any drug can be administered by this route. Can be used to draw laboratory tests. Rapid infusion in adults is not really feasiblesimilar to a 20-22 gauge IV, but a small IV is better than no IV.
References
1. Fleisher, L.A., et al., ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery. Circulation, 2007. 116(17): p. e418-99. Anderson, J.L., et al., ACC/AHA 2007 guidelines for the management of patients with unstable angina/non ST-elevation myocardial infarction. Circulation, 2007. 116(7): p. e148-304. Antman, E.M., et al., 2007 Focused Update of the ACC/AHA 2004 Guidelines for the Management of Patients With STElevation Myocardial Infarction. Circulation, 2008. 117(2): p. 296-329. Hazinski, M.F., et al., Major changes in the 2005 AHA Guidelines for CPR and ECC: reaching the tipping point for change. Circulation, 2005. 112(24 Suppl): p. IV206-11. Morley, P., Adult Cardiopulmonary Resuscitation in 2007, in Australasian Anaesthesia 2007, R. Riley, Editor. 2007, ANZCA: Melbourne. p. 9-17. Deakin, C.D. and J.P. Nolan, European Resuscitation Council guidelines for resuscitation 2005. Section 3. Electrical therapies: automated external defibrillators, defibrillation, cardioversion and pacing. Resuscitation, 2005. 67 Suppl 1: p. S25-37. Nolan, J.P., et al., European Resuscitation Council guidelines for resuscitation 2005. Section 4. Adult advanced life support. Resuscitation, 2005. 67 Suppl 1: p. S3986. Association, A.H., 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Part 7.2: Management of Cardiac Arrest. Circulation, 2005. 112: p. IV-58-IV-66. Hernandez, C., et al., C.A.U.S.E.: Cardiac arrest ultra-sound exam--a better approach to managing patients in primary non-arrhythmogenic cardiac arrest. Resuscitation, 2008. 76(2): p. 198-206. Handley, A.J., et al., European Resuscitation Council guidelines for resuscitation 2005. Section 2. Adult basic life support and use of automated external defibrillators. Resuscitation, 2005. 67 Suppl 1: p. S7-23. Runciman, W.B., et al., Crisis management during anaesthesia: cardiac arrest. Qual Saf Health Care, 2005. 14(3): p. e14. ILCOR, 2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Part 2:
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Adult basic life support. Resuscitation, 2005. 67(2-3): p. 187-201. Soar, J., et al., European Resuscitation Council guidelines for resuscitation 2005. Section 7. Cardiac arrest in special circumstances. Resuscitation, 2005. 67 Suppl 1: p. S135-70. Association, A.H., 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Part 7.5: Postresuscitation Support. Circulation, 2005. 112(24): p. IV-84-IV-88. Morris, R.W., et al., Crisis management during anaesthesia: hypotension. Qual Saf Health Care, 2005. 14(3): p. e11. Atlee, J.L., Perioperative cardiac dysrhythmias: diagnosis and management. Anesthesiology, 1997. 86(6): p. 1397-424. Thompson, A. and J.R. Balser, Perioperative cardiac arrhythmias. Br J Anaesth, 2004. 93(1): p. 86-94. Association, A.H., 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Part 5: Electical Therapies. Circulation, 2005. 112(24): p. IV-35-IV-46. Association, A.H., 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Part 7.3: Management of Symptomatic Bradycardia and Tachycardia. Circulation, 2005. 112(24): p. IV-67-IV-77. Fuster, V., et al., ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation. Circulation, 2006. 114(7): p. e257-354. Mann, C.J., S. Kendall, and G.Y. Lip, Acute management of atrial fibrillation with acute haemodynamic instability and in the postoperative setting. Heart, 2007. 93(1): p. 45-7. Sulke, N., F. Sayers, and G.Y. Lip, Rhythm control and cardioversion. Heart, 2007. 93(1): p. 29-34. Kalra, L. and G.Y. Lip, Antithrombotic treatment in atrial fibrillation. Heart, 2007. 93(1): p. 39-44. Delacretaz, E., Clinical practice. Supraventricular tachycardia. N Engl J Med, 2006. 354(10): p. 1039-51. Salukhe, T.V., D. Dob, and R. Sutton, Pacemakers and defibrillators: anaesthetic implications. Br J Anaesth, 2004. 93(1): p. 95-104. Cook, D.J., P.R. Housmans, and K.H. Rehfeldt, Valvular Heart Disease: Replacement and Repair, in Kaplan's Cardiac Anesthesia, J.A. Kaplan, Editor. 2006, Elsevier Saunders: Philadelphia.
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Christ, M., et al., Preoperative and perioperative care for patients with suspected or established aortic stenosis facing noncardiac surgery. Chest, 2005. 128(4): p. 2944-53. Poliac, L.C., M.E. Barron, and B.J. Maron, Hypertrophic cardiomyopathy. Anesthesiology, 2006. 104(1): p. 183-92. Howell, S.J., J.W. Sear, and P. Foex, Hypertension, hypertensive heart disease and perioperative cardiac risk. Br J Anaesth, 2004. 92(4): p. 570-83. Paix, A.D., et al., Crisis management during anaesthesia: hypertension. Qual Saf Health Care, 2005. 14(3): p. e12. Allman, K.G., A.K. McIndoe, and I.H. Wilson, eds. Emergencies in Anaesthesia. 2005, Oxford University Press: Oxford. Selim, M., Perioperative stroke. N Engl J Med, 2007. 356(7): p. 706-13. Association, A.H., 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Part 9: Adult Stroke. Circulation, 2005. 112(24): p. IV-111-IV-120. Singleton, R.J., et al., Crisis management during anaesthesia: vascular access problems. Qual Saf Health Care, 2005. 14(3): p. e20. Miller, L., G.C. Kramer, and S. Bolleter, Rescue access made easy. Journal of Emergency Medical Services 2005. 30(10): p. suppl 8-18. Schwartz, D., et al., The use of a powered device for intraosseous drug and fluid administration in a national EMS: a 4year experience. J Trauma, 2008. 64(3): p. 650-4; discussion 654-5. Orlowski, J., et al., Comparison study of intraosseous, central intravenous, and peripheral intravenous infusions of emergency drugs. Am J Dis Child Volume 144, Issue 1, 1990, Pages 112-117.
36
Airway Emergencies
AIRWAY EMERGENCIES
Assoc Prof Leonie Watterson Dr Adam Rehak
This module aims to assist you in developing: A routine approach to your anaesthesia practice that reduces the likelihood that you will encounter airway difficulties. A systematic approach to recognising and responding effectively when difficulty with the airway arises. The learning outcomes are know-how regarding: Primary, contingency and emergency planning in airway management. Decision-making to support best practice in primary planning. Contingency plans for difficult intubation, using the Difficult Airway Society (DAS) algorithms as an example. Emergency plans for the obstructed airway and compromised ventilation. Procedural knowledge relevant to Bedside manoeuvres to assist intubation by direct laryngoscopy. Intubation by indirect methods including the intubating laryngeal mask airway (ILMA) and alternatives to intubation, such as ventilation via the Proseal laryngeal mask airway. The emergency surgical airway in conjunction with an obstructed airway.
Overview
Good practice in anaesthesia is underscored by careful planning and preparation, early recognition of problems and know-how regarding effective interventions. Prior to commencing anaesthesia the well prepared anaesthetist plans for expected and unexpected events. 1) The primary plan is the preferred anaesthetic technique, reflecting best practice according to available evidence and tailored to the patients needs. 2) It is also practical and worthwhile to plan for a small number of contingencies. These include failure of the primary plan and complications for which there is a reasonable index of suspicion. Contingency plans can also be tailored to the known needs of the patient and surgery. 3) Emergencies, which are unanticipated and unlikely, can potentially develop during anaesthesia. It is not practical to formulate tailor-made plans for each of these. However, human factors research informs us that overreliance upon instinctive pattern recognition and problem solving may contribute to suboptimal management of these situations 1, 2, 3. Emergency plans are simple pre-rehearsed algorithms and decision-support tools that support our clinical judgment and provide structure and logic to our management of these events.
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Airway Emergencies
The Primary Plan For Airway Management

Your preferred approach to a case is your primary plan. It reflects best practice tailored to the individual patients needs, intended surgery and operating environment. A decision-support tool is shown in Box 1.
1. 2. 3. 4. 5. Assess your patient and situation Analyse your options in terms of risks and benefits Make a provisional plan Road-test this with medical and nursing colleagues Revise if necessary
Table 1 summarizes the incidence of various problems encountered during tracheal intubation. It should be noted that the definitions for difficult intubation and mask ventilation used by the American Society of Anaesthetists Task Force on Management of the Difficult Airway assume the operator is a conventionally trained anesthesiologist. The incidence of these problems may be higher for trainees6.
Problem Intubation requiring several attempts or different blades Intubation possible, but Cormack and Lehane Grade IV Intubation impossible Intubation and ventilation impossible leading to cerebral damage Incidence (%) 1-18 1-4 0.05-0.35 0.0001-0.02
Box 1: Steps in planning your anaesthetic technique
Assessing the airway The greatest risk associated with airway management is failure to oxygenate4. This follows airway obstruction or inadequate gas exchange in the presence of a patent airway. Many anaesthetists are particularly concerned with these occurring during induction of anaesthesia, however these can occur under a range of circumstances both within and remote from the operating theatre. The incidence of difficult intubation varies between studies and with the definitions used. It is commonly classified in terms of Cormack and Lehanes grading of the view obtained during direct larygoscopy5 (figure 1 (b)).
Table 1. Incidence of difficult intubation according to the problem encountered (From Crosby et al6).
Assessment for difficult intubation Prior examination of the airway assists in predicting the view during laryngoscopy. Mallampati and co-workers reported a correlation between the oropharyngeal structures observed during mouth opening and the degree of difficulty of laryngeal exposure obtained at laryngoscopy. This was subsequently modified by Samsoon and coworkers7 (fig 1(a)). Mouth opening is now considered to be an imprecise predictor of difficult intubation when used alone, but increases in sensitivity and specificity when other markers are present6,7,8,9,10. Further research has identified additional predictive signs. These are presented below. Mallampati III-IV Limited neck extension Thyromental distance <6cm (figure 2) Inability to thrust jaw forward past upper teeth Short neck Prominent teeth, natural teeth in elderly
Figure 1. (a) Mallampati classification modified by Samsoon and Young. Class I tonsillar pillars visualised, Class II entire uvula visualised, Class III only the base of the uvula visualised, Class IV - only the hard Palate is visualised. (b) Laryngoscopic grade according to Cormack and Lehane. Grade 1 the entire glottic orifice is seen, Grade II only the posterior aspect of the glottic orifice is seen, Grade III the glottic orifice is not seen, Grade IV the epiglottis is not seen (from Samsoon and Young 7).
A proportion of patients with a difficult intubation have no identified clinical predictors. This figure is reported to be as high as 16.3%11. Inspection of records of previous anaesthetics may reveal a history of difficult intubation in some of these patients.
38
Airway Emergencies
due to upward transmitted pressure from the gravid uterus. Pre-eclampsia creates additional risks if oedema affects the airway. Pregnant patients are at risk of pulmonary aspiration pneumonitis as a consequence of their more acidic gastric juices and a greater tendency to regurgitation, compared to non-pregnant patients. Conditions causing bony restriction Rheumatoid arthritis Ankylosing spondylitis In these conditions an otherwise normal larynx may sit anteriorly because restricted movement in the cervical spine or temporomandibular joint limits the laryngoscopes capacity to elevate the tongue. Conditions associated with oedema Angioneurotic oedema Postoperative bleeding Recent intubation trauma Acute burns Oedema may involve the tongue or laryngeal inlet causing obstruction. At laryngoscopy, the laryngeal structures may be within view, but unrecognizable from the surrounding tissue due to oedema. These patients prefer to be nursed sitting up and may develop symptomatic airway obstruction if laid supine so careful evaluation of the airway in the supine position is worthwhile. See emergency plans for management strategies. Conditions causing soft tissue tethering or displacement of the larynx Airway radiation Airway tumours Previous airway surgery Retrosternal goitre Tethering may cause the larynx to deviate from the midline and may also limit elevation of the tongue and pharyngeal soft tissue. Tumours may displace or rotate the larynx, distorting its normal appearance. Tumours may also cause oedema and may bleed, if friable. Tumours, retrosternal goitres and mediastinal masses may compress the intrathoracic trachea when the patient is laid supine or administered muscle relaxants. This creates a high risk for a cant intubate, cant ventilate situation. Assessment of the airway in the supine position is useful in these patients.
39
Figure 2. The Savva and Patil measurements indicating critical distances. The head is fully extended on the neck 9 .
Assessment for airway obstruction or inability to ventilate via bag and mask Signs which may herald difficulty maintaining a patent airway with a sealed face mask include: A short neck A thyromental distance less than 6 cm Excessive head and neck fat Beards Edentulous Special Risk Groups A number of conditions are associated with difficult intubation and/or airway obstruction. Landmarks for a surgical airway may also be obscured in some of these conditions. Obesity and sleep apnoea These commonly occurring conditions can be associated with redundant pharyngeal soft tissue which contributes to airway obstruction when the patient is asleep or sedated. Elevation of the tongue and soft tissues during laryngoscopy may also be more difficult than usual11. Pregnancy Pregnant patients are reported to have an incidence of failed intubation which is tenfold higher than the non-pregnant population 12,13,14,15 . The larynx may be relatively anterior
Airway Emergencies
Airway Trauma Blunt trauma may cause oedema and bleeding associated with facial fractures contributing to difficulty with mask ventilation and intubation. Penetrating injuries may cause distortion of the normal anatomy so that visualisation of the larynx is difficult. The anterior aspect of the neck may be involved in the trauma which limits the surgical airway as a fallback. The patients should be considered to have an unstable cervical spine, until cleared. They are often unfasted and at risk of aspiration of stomach contents. Assessing other factors The risk of preventable emergencies is increased when other factors are not favourable 1, 2, 3 . These should be incorporated into your decision-making. (See Figure 3).
i) How experienced are the people in your team? ii) Do you know the layout of the environment and location of equipment? 4) Are the environmental conditions favourable? i) Will the conditions create additional difficulties? These include: the time of day, location and ambient conditions (noise, lighting, access to the patient). 5) Are you competent to use this approach? i) How experienced are you? ii) What factors are impacting upon your performance during this case? Are you distracted or fatigued? Analysing risks and benefits Each of the factors you consider in your assessment should be weighted according to the magnitude of risk they pose. For instance a patient predicted to be difficult to intubate poses less of a risk than a patient predicted to be impossible to oxygenate with a bag and mask. General anaesthesia with muscle relaxation is an acceptable technique for elective surgery in the former situation, assuming the patient can be easily oxygenated. However it is not likely to be a safe technique in the latter situation. The relative risk is offset by other factors, listed above. For example, the decision to awake the patient following failed intubation for lower segment caesarean section is influenced by the status of the foetus, assuming the patient can be oxygenated by mask or laryngeal mask airway. The provisional plan After assessment of the patient and consideration of the risks and benefits, a provisional primary plan is selected. This is only a provisional plan because road-testing the plan (see later) may alter your choice of technique. This provisional plan may involve any of the following techniques:Regional anaesthesia Consider whether neuraxial anaesthesia, peripheral nerve blockade or infiltration with local anaesthesia is an appropriate technique. General anaesthesia: spontaneous ventilation and non-intubation techniques Patients requiring general anaesthesia who are at low risk of aspiration may be suitable for a spontaneous breathing technique, using face
40
Patient Surgery You
Airway Risks
Resources Environment
Figure 3: Situational factors potentially contributing to the difficult airway
1)
Who is the Patient? i) Is the patient at risk of aspiration? ii) Does the patient have co-morbidities or preferences relevant to choice of anaesthetic technique? 2) What surgical factors are relevant? i) Are there requirements for muscle relaxation and mechanical ventilation? ii) Will you have access to the airway? iii) What is the expected duration of surgery and blood loss? iv) Does the surgeon have individual preferences? 3) Who are you working with and what resources do you have?
Airway Emergencies
mask or standard laryngeal mask airway (LMA). The Proseal LMA contains an oesophageal port enabling insertion of a gastric tube and drainage of gastric contents. A number of reports support the designers claim that it provides better protection against aspiration than the standard LMA, making it a suitable technique in some circumstances where the LMA is considered a relative contraindication16, 17, 18. Mechanical ventilation via the LMA or Proseal LMA is also reported to be a safe and effective technique in well selected patients19, 20, 21. General anaesthesia: endotracheal intubation There are numerous indications for endotracheal intubation including: reduce the risk of aspiration, optimise gas exchange, or enable a range of surgical requirements. Endotracheal intubation is usually achieved via direct laryngoscopy unless failed intubation is highly anticipated. Indirect methods can be employed as the primary plan when difficult direct laryngoscopy is anticipated and the anaesthetist is confident the patient can be adequately oxygenated with bag and mask ventilation. Numerous devices have proven effective in achieving indirect intubation. The intubating LMA (ILMA) has been evaluated in a number of studies, and has a reported success rate 95.7% when used in patients without difficult airways22. It has also been used successfully in patients who are anticipated to be difficult to intubate 23,24,25. Success rates with the ILMA are improved when combined with a flexible fibreoptic bronchoscope 26. An increasing range of techniques employing light wands or fibreoptic video-enhanced laryngoscopes is also available 27,28,29. Awake intubation techniques Patients who have been assessed and considered unsuitable for intubation under general anaesthesia may be managed using awake spontaneously breathing techniques such as fibreoptic bronchoscopy 30. A comprehensive presentation of these techniques is beyond the scope of this chapter. In principle, anaesthetists should obtain as much training and experience as possible under elective conditions, to acquire knowhow with airway management techniques and devices.
Road-testing and revising your primary plan Before you embark upon your plan you should road test it. You might consult a colleague or supervisor. Consultation with the surgical team can greatly improve choice of technique, particularly when the anaesthetist is unfamiliar with the proposed surgical procedure or surgical team. It is also good practice to consult your assistant. The plan may not be workable due to equipment, staffing or other issues not apparent to you.
Contingency Plans
In the event of failure of the primary plan, the contingency plan is the back-up approach which you have decided to adopt if the primary plan fails or complications develop. Contingency plans require specific knowledge of the patient and situation. They will be most effective when they are easy to employ and include clear criteria to guide their use. Example: Difficult intubation These principles are exemplified in algorithms recently recommended by the Difficult Airway Society (DAS) to guide management of difficult and failed intubation 31. They are not intended to prescribe management of all cases of difficult intubation; instead they provide a plan for some specific, potentially serious situations occurring in the adult, non-obstetric patient. The algorithms use a common structure, comprising four sequential plans (labelled A-D). Their starting point is when intubation is found to be difficult during direct laryngoscopy in conjunction with general anaesthesia (Figure 4). In this context plan A, or tracheal intubation via direct laryngoscopy, represents the primary or preferred approach, as discussed in the previous section. Conditions for intubation should be optimised as part of the primary plan, and specific bedside manoeuvres should be employed to deal with the difficult intubation. Only after this best attempt should a failed intubation be declared. Before progressing to the Plan B, the anaesthetist should confirm he or she is able to ventilate the patient with a bag and mask.
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Airway Emergencies
Figure 4: Basic structure of DAS unanticipated difficult intubation flow-chart.
42
Airway Emergencies
The best attempt at intubation Optimising conditions and dealing with difficult intubation before declaring it failed. The larynx should be intubated with as few as possible attempts at laryngoscopy. As such, conditions should, where possible, be optimised to allow the first attempt to be a best attempt. This applies during any intubation, but is particularly important where difficulty is anticipated. A number of strategies have been recommended. These are summarised in Box 2.
Box 2: Bedside strategies to improve success with direct laryngoscopy 1. Optimise conditions before induction a. Have equipment available and checked b. Optimise bed height c. Elevate head into the "sniffing position" d. Educate your assistant in respect to the plan, the technique and use of equipment 2. Consider calling for assistance (preferably from an experienced anaesthetist) 3. Improve the view of the larynx a. Ensure the muscle relaxant is working optimally (assuming it is appropriate to employ these agents) b. Manipulate cricoid pressure. Return a larynx, deviated by cricoid pressure, to the midline. Reduce or remove cricoid pressure if this is distorting the view of the larynx c. Apply optimal external laryngeal manipulation d. Ensure an appropriate type and size of laryngoscope is used. Consider an alternative blade size or type (e.g. McCoy) 4. Negotiate the ETT through a partial view of the larynx a. Rotate the ETT 90 degrees anticlockwise b. Place an introducer through the ETT (do not project past the end) c. Ask an assistant to sublux the angle of the jaw forward d. Convert to a smaller size ETT 5. Intubate with a bougie
view of a midline larynx and cause airway obstruction32,33. It may be worthwhile asking your assistant to lessen the cricoid by half, or even remove it altogether if the best view obtained is inadequate or the patient is difficult to ventilate by bag and mask. Optimal external laryngeal manipulation (also known as BURP - Backward Upright Rightward Pressure) is achieved by placing the flattened fingers on the anterior aspect of the neck over the thyroid cartilage and pushing in the direction described above. This is intended to bring the posterior aspect of the larynx into view 34,35 . Intubating with a bougie. The bougie may be more effective than an introducer when the best view of the larynx is grade 3 36. The bougie is considered most effective when the tip is bent to 60 degrees 37. Intubation over a bougie or a fibreoptic scope is facilitated if the laryngoscope is kept in the mouth 38, the ETT is small 40,41 and rotated 90 degrees anticlockwise 42. Bougies and introducers may be less effective when the larynx is deviated from the midline. It is worthwhile examining CT scans prior to induction, to gain an understanding of the position of the larynx. A distorted laryngeal inlet may be identified by observing gas bubbles escaping from it. Gas bubbles can be generated a gentle forced exhalation achieved by an assistant by applying controlled pressure to the chest wall, synchronised with direct laryngoscopy.
Declaring the intubation failed Unfortunately there is no consensus among the published guidelines strictly recommending when an intubation should be declared failed by direct laryngoscopy 6,8,31,43. A number of the steps outlined above can be employed during a single attempt at laryngoscopy, however more than one attempt may be required. As a rule of thumb you should desist if the SpO2 falls below 90%, check that the patient can be ventilated, and restore the SpO2 to above 95% before the next attempt. Airway swelling and compromised oxygenation may occur as a result of multiple repeated intubation attempts. Thus your
43
Modifying cricoid pressure. The larynx can be inadvertently displaced to the contralateral side by an over-enthusiastic assistant. It is worth asking your assistant to gently move the larynx from side to side, if you cannot identify the midline structures. Ensure he or she is directing pressure directly backwards with pincered fingers. Cricoid pressure can also limit the
Airway Emergencies
contingency plan should also guide the maximum number of attempts that are appropriate before you declare the intubation failed. The ASA Task Force defines difficult intubation as occurring when proper insertion of the tracheal tube with conventional laryngoscopy requires more than three attempts or more than 10 mins. 43 The DAS recommends a maximum of four attempts following a routine induction and three attempts following a rapid sequence induction31, before intubation is declared failed. Fewer attempts may be appropriate, particularly if the operator is inexperienced, when there is evidence of trauma, or where conditions cannot be improved between subsequent attempts.
Dealing with the failed intubation The DAS Plan B and C represent the contingency plans for declared failed intubation. The DAS advises different responses for three specific situations involving unanticipated difficult intubation. The flow-charts for each of these situations can be found in the appendix to this chapter: 1. During elective surgery where the risk of aspiration is low. Here Plan B involves attempting tracheal intubation via indirect methods, including those mentioned previously in the section addressing the primary plan (unless the surgery can safely proceed without endotracheal intubation). Plan C should be adopted if ventilation becomes compromised. Plan C involves cancelling elective surgery, oxygenating the patient by bag and mask ventilation and awakening him or her as soon as muscle relaxation is reversible 2. During rapid sequence induction. In this setting the high aspiration risk and shortened duration of muscle relaxation provided by suxamethonium make secondary attempts at intubation both more difficult and inherently dangerous. The DAS guidelines suggest, therefore, omitting plan B and proceeding immediately to awake the patient (Plan C). A caveat to this recommendation is the situation where the risks of not proceeding with the surgery exceed the risk of continuing without an endotracheal tube. Here ventilation via a Proseal LMATM, a standard LMATM or a sealed face mask for the duration of the procedure may be more appropriate than
aborting the procedure. Cricoid pressure should be maintained, providing it is not interfering with adequate oxygenation. 3. Failed intubation, increasing hypoxia and difficult ventilation. This describes the transition from a cant intubate - can ventilate situation to a cant intubate, cant ventilate situation. As part of our routine practice, anaesthetists commonly manage partially obstructed airways with basic airway management and a range of simple airway devices including: oropharyngeal and nasopharyngeal airways, optimal two-handed face mask ventilation and LMAs. Because invasive rescue procedures are technically difficult and are associated with serious complications, the basic non-invasive strategies should be employed to maximum effect before progressing to the invasive rescue strategies outlined in Plan D. DAS Plan D involves the implementation of invasive rescue techniques in the setting of a cant intubate, cant ventilate situation. These include cannula cricothyroidotomy and the emergency surgical airway. The timecritical, last resort nature of plan D suggest that plan D, and the transition from Plan C to Plan D, are more representative of emergency planning. Consequently these are elaborated in the following section, Emergency Plans. While the DAS algorithm presents each of Plan A-D as discrete phases, in practice, we may ventilate with a bag and mask on several occasions during airway management and may, on occasion, move to and fro between these phases. As previously stated, these algorithms are designed for specific situations and carry certain assumptions. In reality, there may also be a number of variations on Plan B and Plan C appropriate for a particular situation. The specific method used is not as important as the forethought that occurs prior to embarking on your primary plan and your preparedness to employ an appropriate contingency plan.
Emergency Plans
As described in the above section, the DAS algorithms (Plan C and D) provide a strategy for managing increasing hypoxia associated with a failed intubation. This section elaborates
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Airway Emergencies
this strategy, also addressing a broader range of situations which can potentially be associated with hypoxia. Hypoxia can be caused by airway obstruction or impaired gas exchange associated with a patent airway. They both occur commonly, and commonly co-exist. One may conceal signs of the other. Failure to distinguish the relative contribution of each may lead to serious morbidity. Your starting point may be one of the following situations: When the patient is not intubated. For example, in the pre-anaesthesia induction room, post-anaesthesia recovery room or outside the operating suite. A sequential approach should be used to identify and treat airway obstruction, followed by treatment of compromised gas exchange. During intubation - A Cant intubate Cant ventilate situation. This follows the same principles as those for unintubated patients. Strategies to manage airway obstruction are addressed in DAS Plans C and D. A variation of the algorithm specific for this situation has been published (Figure 5). Following intubation, where there is a concern about ventilation or oxygenation. This situation may occur during induction, maintenance, or emergence from anaesthesia, during transport of critically unwell patients, or in patients who have been intubated outside of the operating theatre environment. Management must include a systematic elimination of problems arising 1) in the ventilation circuit (above the airway), 2) in the breathing tube (in the airway) and 3) with ventilation or gas exchange (below the airway). This situation is addressed further in the chapter on Anaesthetic Emergencies.
inlet or trachea by an inflammatory mass, haematoma or other discrete mass. The features of airway obstruction are shown in Box 3.
Box 3: Recognition of Upper Airway Obstruction Look, Listen & Feel for: Consider patient unstable if *: Chest wall excursion Absent or see-saw Expired gases Reduced Oxygen saturation SpO2 < 90% Functional Obstruction (sedation, narcotisation, coma) Anatomical Obstruction (post surgical swelling,) haematoma, foreign body, traumatised larynx) Sedated or comatose Snoring, periodic breathing
Patient alert,sits forward Dysphagia, dysphonia, dribbling Reduced airflow rate Stridor (supraglottic obstruction) Prolonged expiratory flow rate > 3 L/sec (tracheal obstruction) * These parameters are presented as a guide. Assessment should take into consideration patient trends and co-morbidities.
Functional Obstruction The immediate response is structured on graded intervention (Figure 5). After each step the patient should be re-assessed. Reversible causes should be excluded. These include foreign body, drug-induced sedation, and residual muscle relaxation. Simple measures should be employed before progressing to invasive rescue measures. These include: 1. Position the head in the sniffing position (neck flexion and head extension). 2. Apply maximum jaw thrust and chin lift. 3. Insert an oropharyngeal or nasophayngeal airway. 4. Ensure a correctly sized mask is used. 5. Reduce leaks around the mask in edentulous patients by abutting the skin around the mouth with the mask (a third hand is required). Leaks around beards may be reduced by applying dressings, such as Op-site, over the beard. 6. If the airway remains obstructed the anaesthetist should use two hands to position the mask and ask an assistant to
Upper Airway Obstruction

In the majority of situations obstruction results from functional reduction in muscle tone in the supraglottic region in a patient who is either pharmacologically sedated, has a reduced level of consciousness or has been administered muscle relaxants. Anatomical obstruction presents less frequently and reflects compression of the pharynx, laryngeal
45
Airway Emergencies
apply positive-pressure ventilation with the bag. 7. Depending upon the circumstances and recent history, it may be appropriate to have a single attempt at intubation via direct laryngoscopy. Conditions should be optimised as described in the section on contingency planning. Further attempts to intubate are less appropriate if repeated unsuccessful attempts to intubate have recently occurred. 8. The LMATM and more recently the Proseal LMATM are recommended as devices to support ventilation in an obstructed
airway44, 45. Some data also supports the efficacy and safety of the Combitube when used appropriately46,47. However the incidence of complications is higher, including oesophageal rupture 48,49. 9. As a final step, an emergency surgical airway via the cricothyroid membrane is recommended. Surgical airways carry significant risks and should only be considered in the event of actual or imminent life threatening hypoxaemia where other options are limited.
46
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Figure 5. DAS Flow-chart for cant intubate, cant ventilate situation.
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Rescue ventilation via cricothyroidotomy or a surgical airway Oxygenation via a subglottic approach is indicated when critical airway obstruction and hypoxaemia exist. Formal tracheostomy and percutaneous tracheostomy are likely to contribute to excessive delays in oxygenation, which will be best achieved with an airway device inserted through the cricothyroid membrane. The goals of treatment are in descending order of importance:- 1) delivery of oxygen, 2) exhalation to avoid gas trapping and facilitate removal of carbon dioxide (CO2) and, 3) protection of the lungs from aspiration of stomach contents or blood. Three approaches are described: cannula cricothyroidotomy with percutaneous transtracheal jet ventilation, surgical cricothyroidotomy with insertion of a cuffed endotracheal tube, and percutaneous cricothyroidotomy via a small diameter uncuffed tube. The first two approaches are more widely recommended 31, 50. Cannula cricothyroidotomy with percutaneous transtracheal jet ventilation This approach may provide temporary oxygenation when the airway is obstructed at the level of the glottis or above. The device is a large bore intravenous cannula inserted through the cricothyroid membrane, in its lower third and directed caudad at 45 degrees to the coronal axis. Identification of the trachea is facilitated by aspirating air via a syringe as the cannula is inserted, and reconfirmed after the cannula is advanced. A low compliance, high-pressure ventilation source (40psi) capable of delivering >40 L/min is necessary 51,52 . This can be delivered by a purposedesigned jet insufflation device. Alternatively, a make-shift system can be assembled using a standard intravenous giving set connected via oxygen tubing to a high pressure oxygen source. Options include direct attachment to a cylinder or wall outlet or connection to the common gas outlet on the anaesthetic machine via a 6mm ETT connector. This approach provides no protection against aspiration. Suboptimal elimination of CO2 is a further disadvantage. Kinking of the cannula will result in obstruction to the gas flow and thus loss of oxygenation. Gas trapping may occur if there is no route for exhalation via the upper airway. Displacement of the cannula can result
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in subcutaneous air. Surgical Cricothyroidotomy Insertion of a cuffed endotracheal tube achieves all the three goals listed above. Ventilation can be achieved via a standard low pressure ventilation device. A small cuffed ETT (6.0 mm OD in an adult) is introduced via a horizontal incision in the lower third of the cricothyroid membrane. Entry can be facilitated by opening the incision with artery forceps or a scalpel handle. The risk of creating a false passage may be reduced if the ETT is passed over a bougie53. Percutaneous Minitracheostomy Percutaneous devices potentially achieve better oxygenation and ventilation than intravenous cannulae. They generally have an internal diameter of 4 mm, the critical diameter needed to achieve an exhalation time of less than 4 seconds54. They achieve high minute volumes using low pressure ventilation circuits. They provide minimal protection against aspiration. Gas may escape upwards through the glottis if it is only partially obstructed and paradoxically, ventilation may be facilitated by not actively achieving patency of supraglottic structures. There are a number of commercially available devices. Operators should acquaint themselves with the components and respective insertion techniques of these kits, which vary. Anatomical Obstruction Patients with airway obstruction caused by discrete supraglottic or glottic masses or swelling are generally alert and will not tolerate the steps suggested in the functional pathway. These patients require early conservative intervention including: 1. Minimum handling. They often prefer to sit forward. 2. Apply O2 therapy via a face mask. 3. Nebulised adrenaline may temporarily reduce oedema, if present, and should be considered. 4. Patients with a haematoma following neck surgery may benefit from release of sutures while preparing for definitive management. 5. If at any time the patient becomes unconscious then treatment should be as described in the preceding section, Functional Obstruction. As with functional obstruction, the emergency surgical airway should be considered if life
Airway Emergencies
threatening hypoxaemia is imminent and other less invasive options are limited. 6. Definitive management by experienced personnel should be expedited. Definitive management may require a further surgical procedure (e.g. exploration of bleeding) or insertion of a tracheal tube until oedema settles. 7. The appropriate anaesthetic technique will depend upon the underlying problem, urgency, co-morbidities and resources. Decision-making should follow appropriate consultation with senior anaesthetists, surgeons, and other specialists depending upon the patient and location. 8. Anaesthesia techniques used to achieve a definitive airway have included: a. Direct laryngoscopy following gaseous induction of general anaesthesia. b. Awake fibreoptic intubation c. Formal tracheostomy or percutaneous tracheostomy under local anaesthesia.
Impaired Gas Exchange Associated With a Patent Airway

Gas exchange can be compromised by numerous conditions. These may be physiologically classified into three groups 55,56,57 : 1. Type I respiratory failure (hypoxaemia without hypercapnoea). Anaesthetic causes include endobronchial intubation, foreign body, atelectasis and pulmonary oedema. Co-morbid conditions include: segmental collapse, atelectasis, pulmonary venous congestion, consolidation and aspiration pneumonitis. Severe V/Q and structural abnormalities of the heart can cause right to left shunt. The cardinal sign is hypoxaemia and an elevated A-a gradient. Respiratory acidosis is typically evident on arterial blood gas analysis. CO2 may be elevated when the V/Q mismatch and hypoxaemia are severe. However, relative hypoventilation may co-exist if the patient is unable to increase his or her minute ventilation to compensate, due to respiratory muscle dysfunction, fatigue or reduced respiratory drive. 2. Type 2 respiratory failure (hypercapnic respiratory failure). Results from a
decrease in minute ventilation. Conditions associated with hypoventilation can involve impaired central or peripheral neurological control of respiration, decreased chest wall compliance, or weakened muscles of respiration. Anaesthetic causes include sedation, chest wall loading, and residual neuromuscular blockade. Co-morbid conditions causing hypoventilation include coma, neurological conditions, myopathies, and increased airway resistance resulting from bronchoconstriction. These disorders are characterised by CO2 retention, evidence of suppressed ventilatory drive, poor chest wall function, hypoxaemia resulting from reduced alveolar ventilation and a normal A-a gradient. Respiratory acidosis is typically evident on arterial blood gas analysis. 3. Space occupying lesions within the pleural cavity. Examples include pneumothorax and haemothorax. Characteristic signs include asymmetric chest wall movement and breath sounds and a deviated trachea. Assessment Signs of impaired gas exchange are shown in Box 4.
Box 4: Recognition of Ventilation Look, Listen & Feel for: Ventilatory drive Increased work of breathing Abnormal breath sounds Compromised Breathing or Consider patient unstable if*: Respiratory rate <5 or >36 bpm Use of accessory muscles
Wheeze with reduced air entry, widespread crepitations Oxygen saturation SpO2 < 90% CO2 retention PaCO2 > 50 mmHg Fatigue Drowsiness, exhaustion *These parameters are presented as a guide. Assessment should take into consideration co-morbidities and trends
The patients level of consciousness and work of breathing are important criteria of severity, however these must be interpreted within the context of the situation and recent trends. For example, drowsiness can represent either the cause or the result of respiratory depression. Treatment A number of specific and non-specific treatments may be useful in supporting this
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group of patients. Treatment should be guided by the functional effects of the problem. The principles of immediate treatment are the same for all patients and fall into four categories: Oxygen therapy. This should be given early to all patients with hypoxia. This can be given at high flow unless there are specific concerns about exacerbating CO2 retention. Under these circumstances the inspired O2 concentration can be restricted with fixed O2 delivery devices or by using nasal prongs at 2-3 L/min. Hypoventilation and low V/Q generally show a good response to O2 therapy. Severe V/Q mismatch causing shunting may show a poor response to O2. Improved alveolar ventilation. This improves oxygen transfer by removing retained CO2 and exchanging this with O2 in the alveoli which is then available for transfer into the blood. It is particularly useful in hypoventilation (Type 2 respiratory failure). It can be achieved by reversing factors that are depressing ventilation (e.g. drugs) and by providing inspiratory pressure support. In the operating theatre we commonly employ intermittent positive pressure ventilation via an endotracheal tube. In other circumstances respiratory support can be more appropriately achieved with noninvasive pressure support via a purposedesigned face mask, such as Bi-level Positive Airway Support (BiPAP). Positive expiratory pressure. This improves oxygen transfer by preventing or reversing alveolar collapse, thereby increasing the surface area for O2 exchange. It may be effective in patients with V/Q mismatch (Type 1, respiratory failure). It can be administered to spontaneous breathing patients via continuous positive airway pressure (CPAP) or as positive end expiratory pressure (PEEP) in association with intermittent positive pressure ventilation or pressure support ventilation. Reverse specific causes. Depending upon the cause and severity of the underlying condition, the patient may require specific targeted treatment as a matter of urgency. Examples include denitrogenation and pleurocentesis for pneumothorax or
administration of bronchodilators manage severe bronchconstriction.
to
Summary
Airway obstruction occurs commonly in the routine provision of anaesthesia. It can be difficult to distinguish from other causes of hypoxia, and several causes may coexist. Forward planning and preparation will avoid or mitigate the consequences of airway obstruction. Responding to more serious events using a rehearsed, systematic approach will improve the anaesthetists performance, and that of the team. In retrospect, the patient will be viewed to have received appropriate care, irrespective of the outcome.
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Appendix 1 : Difficult Airway Society Algorithms
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52
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Appendix 2 : Surgical Airway Anatomy

The cricothyroid membrane is directly subcutaneous to the skin. It is about 9mm in height and 3cm in width. It usually lies one to one and a half fingerbreadths below the laryngeal prominence. Alternatively it can be located by placing your small finger into the patients suprasternal notch, followed by placement of the ring, long, and index finger adjacent to each other in a stepwise fashion up the neck, with each finger touching the one below it. When the head is in the neutral position, the index finger is usually on or near the cricothyroid membrane. Structures at risk of injury - The cricothyroid membrane is often crossed horizontally in its upper third by the superior cricothyroid arteries. To minimise the possibility of bleeding, the cricothyroid membrane should be incised in its inferior third. The anterior jugular veins run vertically in the lateral aspect of the neck and thus also escape injury. Because the vocal cords are usually located one cm or more above the cricothyroid space, they are not usually injured during emergency cricothyroidotomy. Choice of techniques Three techniques are described: 1) Transcricoid jet ventilation via an intravenous cannula, 2) Conventional ventilation via a purpose designed percutaneously inserted minitracheostomy catheter (internal diameter size 4mm) 3) Conventional ventilation via a small cuffed endotracheal tube, inserted via a scalpelmade incision through the cricothyroid membrane. Each technique is acceptable. The DAS now recommends (1) or (3) over (2). The choice of technique should be made on the basis of the risks and benefits of each technique, the patients circumstances, the operators experience and resources available. Risks and benefits The benefits, in order of importance are oxygenation, gas exchange and protection of the lungs from aspiration of stomach contents.
The risks of these procedures can be divided into insertion problems and ventilation problems. Insertion problems include: Bleeding and difficulty passing the airway device. Damage to the larynx, trachea, or surrounding structures (arteries, veins, oesophagus, pleura). Ventilation problems include: Ineffective ventilation and barotrauma. If the airway obstruction is in the mid to lower trachea or bronchus, none of the catheters used in these techniques will be long enough to bypass the obstruction. A rigid bronchoscope may be the only means to bypass obstruction. Transcricoid jet ventilation by an intravenous cannula Technique In order to perform cannula cricothyrotomy you must first firmly fix the trachea firmly between your thumb and middle finger. You could consider using a 22g seeker needle first to locate the air tube in patients with difficult anatomy. After feeling for the cricothyroid membrane insert the cannula with a 2ml syringe attached through the membrane at an angle of 45 degrees towards the feet. As soon as you can aspirate air, slide off the cannula off the stylette, until the hub reaches the skin, then, remove the stylette and syringe. Check that you can still aspirate air from the cannula. You must never let go of the cannula because it is extremely difficult to secure and maintain in the proper position. Risks Displacement of the cannula may result in subcutaneous air (this will remove all your landmarks making it impossible to find the cricothyroid membrane). Kinking of the cannula will result in obstruction to the fresh gas flow and loss of ventilation. This is more likely with smaller cannulae. The skin is one of the main causes of catheter-kinking, so a small skin incision is recommended before cannula insertion. Advantages It can be used to temporarily oxygenate patients. Anaesthetists may be more confident than with the other two techniques. Disadvantages Gas exchange is inferior to the other two techniques.
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Airway Emergencies
It provides no protection against aspiration Ventilation circuit and equipment Ventilation must be achieved via low compliance circuit attached to a high pressure oxygen source (40psi) capable of delivering >40 l/min. Several options exist including commercially available purpose designed jet insufflator or adapting ready-at-hand equipment. The key components comprise: non-compliant tubing (standard IV giving set, green oxygen tubing); a release valve for exhalation (cut off tubing bung, 3 way tap, etc) and a connector to O2 source (IV sets will connect to green O2 tubing; green O2 tubing can be connected to the common gas outlet of an anaesthetic machine via a connector for paediatric circuits, or a size 6 ETT connector). Management You must see the chest rise and fall as in normal resting ventilation. Continue to maximise the patency of the upper airway by allocating a skilled person to deliver continuous O2 via a face mask (so that any entrained air will be oxygen rich) in addition to airway opening manoeuvres (nasal and Guedel airways, jaw thrust and head tilt). Manage complications: Percutaneous Minitracheostomy. Technique There are a number of Percutaneous Minitracheostomy sets on the market, size ranges from 4mm in diameter and larger. Some of the larger tubes have cuffs and the tube lengths also vary with different makes. Some kits combine the dilator and introducer all in one (Melker), this means one less time consuming manoeuvre. You should be familiar with your hospitals device. First locate the cricothyroid membrane with index finger and hold the trachea firmly between thumb and middle finger. Make a vertical skin incision over the cricothyroid membrane, this can be easily extended up or down if the relationship of the skin with cricothyroid membrane changes. It is recommended that the skin incision be made first for two reasons:- the 16g cannula is more likely to kink if there is no skin incision, making it difficult to pass the guide wire. Secondly, the dilator will not advance though intact skin. After the skin incision, the 16g cannula or 16g needle is inserted 45 caudally
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with a syringe attached. The airway is positively identified by air aspiration. The floppy end of the guide wire is then inserted thought the cannula or needle, the later is then removed leaving only the wire in the airway. A dilator is then passed over the wire into the airway, after this has been removed the catheter and introducer are advanced together into the airway with a slight rotatory motion. The catheter is advanced over the introducer into the airway and then the wire and introducer are removed. This technique is similar to central venous line cannulation. Most kits have no cuff, so they do not provide any airway protection. Secure catheter with suture or trachy tape. Suction down to maintain patency. Risks Some Percutaneous Minitracheostomy kits have a short catheter, which is liable to dislodge with patient movement especially in patients with short obese necks. The smaller size 4 catheters are quicker and easier to place than a larger cuffed size 6 catheter, because less dilatation of the cricothyroid membrane is needed. In hypoxic patients time is of the essence so we recommend using an uncuffed 4mm catheter. If ventilation is found to be inadequate with a 4mm catheter (because the inspired gas is escaping via the mouth) a jet insufflator can be used to achieve adequate ventilation. Advantages Oxygenation and gas exchange achieved, depending on internal diameter of cannula Disadvantages Uncuffed ETTs provide no protection form aspiration however airway protection can be improved with a pharyngeal pack. Ventilation circuit and technique Assuming a cannula internal diameter of 4mm or greater, ventilation is achieved with a standard anaesthetic circuit. Ventilation will be reduced if gas leaks retrogradely through a patent airway. So adequate inspiration is only achieved if the upper airway is obstructed, either through disease or artificially by allowing the tongue to fall backwards and obstruct the upper airway. Surgical Cricothyroidotomy. Technique Try to keep head fixed in the midline by helper (inline stabilisation). Fix thyroid cartilage
Airway Emergencies
firmly so that it does not move when patient moves. Make horizontal incision though the lower third of cricothyroid membrane and then dilate this incision with the handle of the scalpel or artery forceps. Insert a small cuffed ET tube though the hole. Bubbles of air will identify the space, blood will also provide lubrication. A bougie can be used and ET tube railroaded over in-order to make a more controlled intubation of the airway without creating a false passage. Risks There is a potential to make the scalpel incision into the wrong structure e.g. carotid artery. Make the incision in the lower third of the space, horizontally. Advantages Achieves oxygenation, gas exchange and protection best of the three techniques Ventilation circuit and technique Ventilation is achieved with a standard anaesthetic circuit.
References
1. Cooper JB, Newbower RS, Long CD, McPeek B. Preventable Anesthesia Mishaps : A study of human factors. Anesthesiology 1978:49:399-406. Howard SK, Gaba DM. Factors influencing vigilance and performance of anesthetists. Current Opinion in Anesthesiology 1998: 11: 651-57. Weingart SN, Wilson RMcL, Gibberd RW, Harrison B. Epidemiology of Medical Error. BMJ 2000;320:774-7. Cheney FW, Posner KL, Lee LA, Caplan RA, Domino KB. Trends in Anesthesiarelated Death and Brain Damage: A Closed Claims Analysis. Anesthesiology 2006: 105; 1081-6 Cormack RS and Lehane J. Difficult tracheal intubation in obstetrics. Anaesthesia 1984 Crosby ET, Cooper RM, Douglas MJ et al. The unanticipated difficult airway with recommendations for management. Can J Anaesth. 1998. 45; 7: 757-76. Cooper SD, Benumof JL. Airway Algorithm: Safety Considerations. Chapter 9 in Patient Safety in Anesthetic Practice. RC Morrell (ED). Churchill Livingstone 1997 Janssens M and Hartstein G. Management of the difficult intubation. European Journal of Anesthesiology 2001: 18: 3-12. Savva D. Prediction of difficult tracheal intubation. Brit J Anaesth, 1994; 73: 149153
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24. Nakazawa K, Tanaka N, Ishikawa S, et al. Using the intubating laryngeal mask airway (LMA-Fastrach) for blind endotracheal intubation in patients undergoing cervical spine operation. Anesthesia and Analgesia 1999; 89: 1319 21. 25. Joo HS, Kapoor S, Rose DK, Naik VN. The intubating laryngeal mask airway after induction of general anesthesia versus awake fibreoptic intubation in patients with difficult airways. Anesthesia and Analgesia 2001; 92: 13426. 26. Pandit JJ, Maclachlan K, Dravid RM, Popat MT. Comparison of times to achieve tracheal intubation with three techniques using the laryngeal mask or intubating laryngeal mask airway. Anaesthesia 2002; 57 128-32. 27. Dimitriou V, Voyagis GS, Brimacombe JR. Flexible light-wand-guided intubation through the ILM. Acta Anaesthesiologica Scandinavica 2001; 45: 263-4. 28. Gorback MS. Management of the difficult airway with the Bullard laryngoscope. Journal of Clinical Anaesthesia 1991; 3: 473-7. 29. Watts AD. Gelb AW. Bach DB. Pelz DM. Comparison of the Bullard and Macintosh laryngoscopes for endotracheal intubation of patients with a potential cervical spine injury. Anesthesiology 1997: 87(6):133542. 30. Ovassapian A(ed). Fibreoptic Endoscopy and the Difficult Airway. Philadelphia: Lippincott-Raven, 1996 31. Henderson JJ, Popat MT, Latto IP, Pearce AC. Difficult Airway Society guidelines for the management of the unanticipated difficult intubation. Anaesthesia 2004; 59: 675-94. 32. Bruin G, Buckley N. Intubating conditions and correct application of cricoid pressure during rapid sequence induction: who should hold the mask? Canadian Journal of Anaesthesia 1997; 44: 900 33. Shorten GD, Alfille PH, Gliklich RE. Airway obstruction following application of cricoid pressure.Journal of Clinical Anesthesia 1991; 3: 403-5. 34. Benumof JL, Cooper SD. Quantitative improvement in laryngoscopic view by optimal external laryngeal manipulation. Journal of Clinical Anesthesia 1996; 8: 13640. 35. Knill RL. Difficult laryngoscopy made easy with a BURP. Canadian Journal of Anaesthesia 1993; 40: 27982. 36. Gataure PS, Vaughan RS, Latto IP. Comparison of the gum elastic bougie and the stylet. Anaesthesia 1996; 51: 935-8
37. Nolan JP, Wilson ME. An evaluation of the gum elastic bougie. Intubation times and incidence of sore throat. Anaesthesia 1992; 47: 878-81. 38. Dogra S, Falconer R, Latto IP. Successful difficult intubation. Tracheal tube placement over a gum-elastic bougie. Anaesthesia 1990; 45: 774-6. 39. Klafta JM. Flexible tracheal tubes facilitate fibreoptic intubation. Anesthesia and Analgesia 1994; 79: 1211-2. 40. Koh KF, Hare JD, Calder I. Small tubes revisited. Anaesthesia 1998; 53: 46-50. 41. Hakala P, Randell T, Valli H. Comparison between tracheal tubes for orotracheal fibreoptic intubation. British Journal of Anaesthesia 1999; 82: 1356. 42. Cossham PS. Difficult intubation. British Journal of Anaesthesia 1985; 57: 239. 43. American Society of Anesthesiologists Task Force on Management of the Difficult Airway. Practice guidelines for management of the difficult airway. An updated report. Anesthesiology 2003; 95: 126977. 44. Parmet JL, Colonna-Romano P, Horrow JC, Miller F, Gonzales J, Rosenberg H. The laryngeal mask airway reliably provides rescue ventilation in cases of unanticipated difficult tracheal intubation along with difficult mask ventilation. Anesthesia and Analgesia 1998; 87: 661 5. 45. Benumof JL Laryngeal mask airway and the ASA Difficult Airway Algorithm. Anesthesiology 1996; 84: 686-99. 46. Baraka A, Salem R. The Combitube oesophageal-tracheal double lumen airway for difficult intubation. Canadian Journal of Anaesthesia 1993; 40: 12223. 47. Klein H, Williamson M, Sue-Ling HM, Vucevic M, Quinn AC. Esophageal rupture associated with the use of the Combitube. Anesthesia and Analgesia 1997; 85: 9379. 48. Richards CF. Piriform sinus perforation during Esophageal-Tracheal Combitube placement. Journal of Emergency Medicine 1998; 16: 379. 49. Vezina D, Lessard MR, Bussieres J, Topping C, Trepanier CA. Complications associated with the use of the EsophagealTracheal Combitube. Canadian Journal of Anaesthesia 1998; 45: 7680. 50. Scrase I, Woolard M. Needle vs surgical cricthyroidotomy: a short cut to effective ventilation. Anaesthesia, 61:962-974, 2006. 51. Dworkin R, Benumof JL et al. The effective Tracheal Diameter That Causes air Trapping During Jet Ventilation. Jr.
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Cardiothoracic Anesthesia 4:731-736, 1990. 52. Ryder IG, Paoloni CCE. Emergency transtracheal ventilation: assessment of breathing systems chosen by anaesthets. Anaesthesia, 51: 764-768. 1996. 53. Morris A, Lockey D, Coats T. Fat necks: modification of a standard surgical airway protocol in the pre-hospital environment. Resuscitation 1997; 35: 253-4 54. Craven RM, Vanner RG. Ventilation of a model lung using various cricothyrotomy devices. Anaesthesia, 59: 595-599, 2004.
55. Wilson MM, Irwin RS. A Physiologic Approach to Managing Respiratory Failure. Chapter 42 in Manual of Intensive Care Medicine, Irwin and Rippe (Eds). Lippincott Williams and Wilkins, 4th Edition, Sydney, 2006. pp251-4. 56. Pozzi E. Gulotta C. Classification of chest wall diseases Monaldi Archives for Chest Disease. 48(1):65-8, 1993. 57. Sharma S. Respiratory Failure. EMedicine, WebMD publishers. http://www.emedicine.com/med/topic2011 .htm [Last Updated: June 29, 2006]
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ANAESTHETIC EMERGENCIES
Assoc Prof Jennifer Weller
Overview
Managing a life-threatening emergency in the operating room can be a daunting prospect. We use complex equipment and monitoring, our patients often have severe underlying pathology, the surgical insult can cause sudden and profound physiological derangement, and the drugs we employ can have impressive and unpredictable side effects. The clinical signs are often poorly defined, there is pressure of time and multiple tasks to perform, making it difficult to think clearly and logically. Although the number of things that can go wrong seems unlimited, adverse events tend to present in a limited number of ways. Our patients frequently present with hypoxia, hypotension or hypertension, rhythm disturbance or ventilation problems. Working out what to do can be challenging in this complex and dynamic environment. Developing a systematic approach to these generic conditions may be a useful strategy to assist diagnosis and management of crisis events. In addition, the teamwork and behavioural factors discussed in the Human Factors Module can be crucial in our ability to implement an effective management plan. The objectives of this module are to: Develop an immediate response to a critical situation. Improve management of crises by optimising the use of the operating room team. Identify behavioural strategies to improve diagnosis. Develop a systematic approach to critical events in the operating theatre.
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Anaesthetic Emergencies
An Immediate Response to a Crisis

As junior doctors we are taught the ABC of resuscitation. Think how often this has come to your rescue. It is a pre-compiled response, widely applicable, it doesnt require thinking, it can be done even in a state of panic, it may yield vital information and it may be lifesaving. Although there is some resistance by doctors to practising by algorithm, there is a time and a place, as illustrated by this simple and memorable resuscitation algorithm. In anaesthesia, the clinical context is altered. We are not dealing with a patient who has spontaneously collapsed, but a patient under anaesthesia. We need to include this in our version of the resuscitation algorithm. Have you ever come to help at a cardiac arrest in theatre and found the patient still receiving volatile agent? The following adaptation of the basic ABC of life support is modelled on David Gabas Initial Response to a Serious Event (Crisis Management in Anesthesiology, 4)
What sort of communication works? Your tone of voice, and the clarity of instruction influence the outcome. Communications should be directed to a specific person. Avoid asking the room in general for a defibrillator. Everyone or no one may go. Its a useful strategy to learn the names of your team. Ensure your requests have been acknowledged and accepted. Conflict can arise. Focus on whats right for the patient, and save the arguments for after. Avoid judgemental comments (What have you done?!) Your team may become less helpful. Listen. Be open to suggestions from the team. What is the role of the leader? Reflect on your role as leader in a clinical crisis in the operating theatre. Your tasks may include decision making, prioritising, organising the team, and re-evaluating the situation. The leader should be the clearing-house of ideas from the team, centralising communication and coordinating the teams activities. The leader should have a global view of whats happening. The problem leader Think of your experience in theatre. What sort of leadership behaviour is likely to cause problems in a crisis? You may include the following: Weak leadership: Failure to take control of the situation: no directions to team, no plan. Authoritarian figure: The team may be afraid to offer suggestions, alternatives or point out problems for fear of the consequences. All-knowing leader: The team may be discouraged from offering input as they assume the leader is all-knowing, all-powerful and doesnt need their suggestions. Think what your ideal leader would behave like. What should the leader be doing? Think of a well-run cardiac arrest call, a wellrehearsed trauma team call, or a major operating room crisis. What has the leader been doing? Standing back allows the leader to take a global view, allows him or her to plan, prioritise and co-ordinate the team. Focusing on one aspect of care such as airway management or vascular access can make it difficult or impossible to take this global view. How do you organise your team? Identify the tasks that need to be done and allocate them appropriately. In netball, it would be a poor plan to put your best goal shooter in defence. In an operating room crisis, sending
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The Anaesthetists ABC

A=Airway and Anaesthesia Check airway. Turn off all anaesthetics in use and double check B=Breathing Give 100% oxygen AND verify Maintain oxygenation at all costs. Consider Ambubag, alternative O2 source C=Circulation ACLS, fluids and vasopressors as necessary. Double-check vasodilator infusions.
Developing Skills in a Working Team

This module provides an opportunity to apply the principles of crisis management described in the human performance module. What does teamwork involve? Think of a sports team. Aspects of teamwork include: communication, leadership, a common goal, a plan, working together, utilising skills of team members. Think how this relates to the operating room team?
Gaba DM, Fish KJ, Howard SK. Crisis Management in Anesthesiology. New York: Churchill Livingstone; 1994.
your tech out for blood instead of the student nurse, getting your anaesthetic colleague to keep a record of the evolving crisis while you put in the central line would also be less than optimal task allocation. Once youve handed out the tasks, check that the team is coping with the tasks theyve been given. Key points of Teamwork: Communicate effectively - Clear, concise, directed - Two-way, open - Centralised Leadership - Stand back, take a supervisory role - Allocate tasks appropriately - Prioritise These skills require practice. Dont wait for the next emergency or next EMAC course. Practice them on a daily at work.
Allocate attention wisely We can only attend to a limited number of pieces of information at once. Its easy to overlook something if were concentrating on one particular task such as inserting a central line or teaching a medical student. Off-load tasks Off-loading tasks can aid problem solving by giving us more thinking space. By allocating a whole task area such as fluid resuscitation or airway management to a colleague, we can take a global view of the crisis. Stand back and take a supervisory role. Verbalise Talking out load can assist your own thinking. Also, as you re-evaluate the problem, you let the other members of the team know what youre thinking, what youve considered and what you cant work out. They are brought up to speed, may see things youve missed or misinterpreted, or come up with a new suggestion. Consider what its like trying to help a junior doctor with an endotracheal intubation if they dont say what theyre seeing, what problem theyre encountering. Its hard to offer suggestions. Share the problem How does a colleague help with diagnosis? They may have a new perspective. A more detached assessment may spot something youve missed. Are certain ways of conveying the problem to responders more useful than others? If, as a helper, were given a description of the event rather than diagnosis we can form our own conclusions. We may avoid going down the same track in a fixation error. Consider how you convey information to a colleague when they come to help. Re-evaluate Did the action plan work? Is the problem getting better? Are there any side effects of treatment? Are there additional problems? Was the initial diagnosis correct? Am I repeating the same interventions and not solving the problem? These considerations may help us detect or avoid fixation errors. Strategies to improve diagnosis Be vigilant Allocate attention wisely Offload tasks Verbalise Share the problem
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Behavioral Strategies to Improve Diagnosis

What can we do to support diagnostic decision making under pressure? Problem solving requires thinking. Although the ability of humans to problem solve is a powerful process, it requires a great deal of mental effort and is vulnerable to stress and overload. Certain behavioural strategies, including re-evaluation and verbalising may assist this process of deductive problem solving. There is some evidence that we make a diagnosis by matching the available information to a pattern in our long-term memory compiled from past experience. With only limited data, we tend to match the problem to approximate to the nearest match. Increasing the available information, may improve the match. How do we gather this information? Vigilance If were not looking, we wont see. Vigilance can deteriorate under such conditions as fatigue, boredom or distraction. Should we consider personal strategies to minimise the effects of these factors, such as routine scanning? Do you have a strategy to combat fatigue?
A Systematic Approach to Crisis Management

In a crisis, we need to gather all the relevant information. Problems arise when we overlook important information. Its easy to miss information in the stress of a crisis. Do we need a system to gather this information to avoid missing something? The presentation is often generic, for example, hypoxia, high airway pressure, abnormal CO2, tachycardia, or hypotension. A simple, memorable systematic approach for these specific generic events could include improve information gathering and diagnosis. An example could be a spatially oriented approach to the identification of the cause of high airway pressure e.g. machinecircuit-airway-lungs-pleural cavity, chest wall. COVER ABCD A SWIFT CHECK (Runciman, 1993) is a well known systematic approach to diagnosis of any adverse event. A written cognitive aid may support memory. What algorithms do you find helpful? First you have to remember them, and do this in the stress of a crisis. Alternatively you could have a written memory aid. A system that makes sense to one person may be an enigma to another. A few generic approaches are suggested in the appendices. You may want to develop your own. It is important to rehearse these algorithms to ensure they can be implemented swiftly and securely when the need arises.
and fixation errors are frequent. You see the information you want in order to confirm your diagnosis. (It is, after all, very uncomfortable not knowing what the problem is.) A systematic review of data may help avoid these errors in cognition. A systematic approach can be rehearsed, promoting a rapid, streamlined performance.
The systematic approach in context

A systematic approach may delay effective treatment. We have all been in a situation where a problem arises; a diagnosis is made in seconds and treatment instituted rapidly and effectively without any consideration of alternative diagnoses. We have a tendency to go for the most likely cause straight away and treat it. This is referred to as frequency gambling. By definition, more often than not frequency gambling pays off. Experience is likely to improve the odds. Delaying the obvious treatment by following a rigid sequence of checks will cause delay. However, frequency gambling only works if we have jumped to the correct conclusion. Persistence with an incorrect diagnosis is an example of a fixation error. (See: Human Performance Issues). If we are convinced of the diagnosis, there is a tendency to only see information that supports that diagnosis (confirmation bias). If a problem is not immediately fixed by addressing the most likely cause, re-evaluate using a systematic approach and make sure something is not being missed. It may even be appropriate to delegate this review to a skilled assistant who may take a more objective approach. A systematic approach may not work for unpredicted events. Another limitation to an algorithmic approach is that we can only make plans for predicted eventualities. A procedures manual will not address an unforeseen event.
Advantages of a systematic approach to diagnosis and treatment in a crisis

A systematic approach covers the likely and or life-threatening causes quickly and comprehensively. Cognition is impaired in a crisis. The use of a rehearsed response reduces the amount of thinking required and may solve the problem. Freezing under fire: an automatic response can provide a fallback routine for the panic stricken. It should at least ensure initial life-saving interventions are instituted. A systematic approach encourages examination of all relevant data and repeated re-evaluation of the situation. Confirmation bias in perception of data,
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Limitations of a systematic approach

Only works if you remember it. Only useful for predicted eventualities. Working through a procedure checklist may delay management.
Rehearsal of systematic approach

A systematic approach needs to become
automatic or were back to the laborious process of thinking from first principles. For each routine case, it could be helpful to mentally rehearse for possible problems. This could also provide an in-theatre teaching option that focuses attention on the case in hand rather than potentially distracting from patient care.
systematic approaches to generic crisis presentations. You may wish to develop your own approaches to these problems.
Suggested Reading
Benumof L, Saidman LJ. Anesthesia and Perioperative Complications. 2nd Ed, 1999, Mosby: New York. Bognor, M. S. Human Error in Medicine. 1994, Lawrence Erlbaum Association Inc: New Jersey. Gaba, DM, Fish, KJ, Howard, SK. Crisis Management in Anesthesiology. 1994, Churchill Livingstone:Philadelphia. Reason, J. Human Error. 1990, Cambridge University Press: Cambridge. Boud D, Keogh R, Walker D. Reflection: Turning Experience into Learning. 1985, Routledge:Abingdon.
Summary
Core knowledge and skills are basic requirements for effective crisis management. In addition to the opportunity for rehearsing for uncommon events, this module aims to explore how to behave in a clinical crisis, and to think about how we think. The simulated events provide an opportunity to practice new strategies. The appendices offer some specific
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Appendices
The Hypoxic Patient Definition of hypoxia:
SpO2 < 90%, PaO2< 60mmHg or SpO2 falling by >=5% Detect cyanosis at SpO2<85%, PaO245-50mmHg Deoxygenated Hb>5gm/100ml Consider: Patient context (high requirement, poor O2 delivery, chronicity of low SpO2, surgical procedure, position, pre-existing diseaserespiratory, cardiac, renal, liver, obesity) Why is the SpO2 below normal or falling? It seems prudent to investigate early Initial response to a crisis: The anaesthetists ABC Treat the hypoxia while looking for the cause Dont assume artefact Verify hypoxia is real Systematic approach to diagnosis of hypoxia: O2 supply Check pressure gauges, vaporizer housing
flow
meters,
FIO2,
Anaesthetic machine Check ventilator: VT, rate, airway pressure gauge Circuit: connections, one-way valves, filter Airway Exclude obstruction: In unintubated airway, filter, and airway devices. Check for secretions. Pass suction catheter down ETT and make sure it goes beyond end of ETT Ventilation Exclude endobronchial intubation, look and listen for bilateral chest expansion, adequacy of minute ventilation, bronchospasm, recheck airway pressure gauge, exclude pneumothorax Lungs Gas exchange problem: aspiration, pulmonary oedema, bronchospasm, consolidation, and atelectasis Pulmonary embolism -air, thrombus, fat Blood Circulation: Low cardiac output Anaemia: Reduced O2 carriage, high O2 extraction and decreased mixed venous PO2 Tissue Uptake Increased metabolism (fever, thyroid crisis, etc)
O2 supply anaesthetic machine circuit airway ventilation lungs blood tissue uptake
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High Airway Pressure

A systematic approach to high airway pressure: Consider the patient context: surgery, preexisting disease, prior events, risk factors. High airway pressure will present in several ways: Problem ventilating the patient (e.g. decreased compliance in breathing bag, poor chest expansion, reduced breath sounds, reduced expiratory tidal volume, abnormal ventilator sound, high airway pressure alarm) Hypoxia secondary to hypoventilation Circulatory collapse due to high intrathoracic pressure (e.g. occluded expiratory limb, tension pneumothorax) Tachycardia Systematic approach to diagnosis of high airway pressure: Gas supply Check O2 bypass/flush/other high pressure gas source Circuit Ventilator/bag switch Obstruction to expiration in circuit, ventilator, scavenger system PEEP valve? Exclude circuit and machine problem by disconnecting and ventilating with self-inflating bag Airway Exclude obstruction: filter, airway, ETT, secretions, foreign body Lungs Bilateral chest expansion? (endobronchial intubation, pneumothorax, haemothorax) Breath sounds? (bronchospasm, endobronchial intubation, aspiration, pulmonary oedema, atelectasis) Surgical Procedure Raised intra-abdominal pressure Surgical intervention Position Pleural cavity pneumothorax, haemothorax Chest wall Inadequate muscle relaxation, opioid induced chest wall rigidity Malignant hyperpyrexia Obesity
gas supply circuit airway lungs pleural cavity chest wall surgical procedure
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Abnormal ETCO2 in the Anaesthetised Patient Increased ETCO2

PaCO2=K x CO2 production Alveolar ventilation Normal upper limit 46mmHg Apnoea results in rise of PaCO2 of 8-15mmHg in first minute, then 3mmHg /min Causes of hypercapnia a) Normal lung function: Exogenous: laparoscopic CO2 insufflation, NaHCO3 administration, inspired CO2 (soda lime exhausted, incompetent valves, rebreathing) Hypoventilation: respiratory depression, increased mechanical load due to decreased compliance or increased resistance in respiratory system, inadequate IPPV Increased CO2 production: fever, sepsis, seizures, hyperthyroidism, TPN. b) Impaired gas exchange mismatch between ETCO2 and PaCO2 Increased anatomic dead space, inappropriate artificial airway. Increased physiological dead space- reduced cardiac output, hypovolaemia, hypotension, pulmonary embolism, COPD Initial response to a crisis: The anaesthetists ABC Systematic approach to raised ETCO2
Inhaled/exogenous CO2 hypoventilation increased production
Inhaled CO2 Check capnograph trace for return to baseline Exogenous Insufflation with CO2, NaHCO3 Hypoventilation ventilator settings, airway pressure, ?obstruction, lungs Increased Production fever, parenteral nutrition, malignant hyperthermia
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Decreased ETCO2
No ETCO2: consider oesophageal intubation, accidental extubation. ETCO2 may not reflect PaCO2 if ventilation is going to unperfused lung, e.g. severe hypotension, pulmonary embolism Erroneously low ETCO2 may be due to air entrainment in the circuit, equipment malfunction. Onus of proof is on the anaesthetist to verify data is erroneous Systematic approach to diagnosis of decreased ETCO2: Airway Oesophageal intubation, accidental extubation Circuit Air entrainment (leak), dilution with circuit gases (sampling problem) Ventilation Ventilator settings, overenthusiastic hand ventilation Gas Exchange Problem Pulmonary embolism, cardiac failure/arrest, severe hypotension Decreased production Hypothermia, hypothyroidism, decreased metabolism
airway circuit ventilation gas exchange decreased production
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Hypertension
The hypertensive, anaesthetised patient is generally responding to a surgical stimulus or has pre-existing hypertension. Specific circumstances may suggest a neurological cause. However, the cause may be a response to hypoxia or hypercarbia, to unintended exogenous administration of a vasoconstrictor, or to phaeochromocytoma. Always include the surgery in your systematic review. If your initial response doesnt work, consider the following sequence: Systematic approach to hypertension: Pre-existing hypertension Treated, untreated, ?medication taken Sympathetic reflex response: Light anaesthesia: is the anaesthetic agent actually being delivered? (Vaporizer leak, IV infusion disconnection/ error) Hypoxia, hypercarbia: check SpO2, ETCO2 Cerebral event: raised ICP, cerebral ischaemia, vasospasm Sympathomimetic effect Exogenous: accidental administration? Endogenous: e.g. phaeochromocytoma Surgical: Aortic clamp
Pre-existing hypertension sympathetic reflex response sympathomimetic effect surgical
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Hypotension
Hypotension is a very common unintended event in anaesthesia practice, most commonly resulting from relative overdose of anaesthetic agents, hypovolaemia or central neural blockade. For severe hypotension, the initial response to a crisis algorithm would be appropriate. Consider treatment before or in the process of diagnosis. If the initial intervention doesnt solve the problem, the following approach may be useful: Systematic approach to hypotension:
Hypovolaemic Cardiogenic Distributive Obstructive
Hypovolaemic Blood loss, fluid deficit Cardiogenic Contractility, rate, dysrhythmia Anaesthetic agent, vasodilators Distributive Vasodilation: drugs, sympathetic block, sepsis, anaphylaxis Obstructive High intrathoracic pressure, tamponade, pulmonary embolus, surgical compression
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Trauma
The Management of Trauma

Dr Tim Gray Dr Richard Morris
The aims of this module are to increase skill and knowledge in the approach to resuscitation and management of the trauma patient in the perioperative period.
Objectives
This module serves as an introduction to many aspects of trauma anaesthesia: The process of early evaluation and resuscitation of the trauma patient. Effectively reviewing the trauma patient on handover from the resuscitation team. Evaluating evolving injuries during anaesthesia care. Coordinating management priorities and effective team behaviours. Responding to specific problems including: - Cervical spine injuries - Intracranial trauma - Trauma related airway problems - Intra cranial trauma - Concealed bleeding - Large volume resuscitation - Cardiothoracic injuries - Complications of long bone and pelvic injuries
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Trauma
Overview
The resuscitation and management of the multiply injured patient can be divided into three phases: Initial resuscitation, definitive management of injuries, ongoing care and recovery. The boundaries between these phases may be blurred considerably. Trauma victims may require anesthesia and surgery while still in the resuscitation phase, occult or evolving injuries may cause acute deterioration during definitive management or subsequent care. Thus it is imperative that anesthetists have a systematic approach to assessment and management of the trauma victim at all stages of management, as well as strategies to deal with specific trauma related anesthetic issues. This module outlines principles well covered in the EMST [Early Management of Severe Trauma] course convened by the RACS. This module does not attempt to replace this course, completion of which is recommended for Anaesthetists who are regularly involved in the management of injured patients.
management can provide important information, but should not take priority over management of life threatening injuries. Prehospital teams may have a system of handover of clinically relevant material. If possible try not to interrupt the paramedic whilst they handover, but listen and save any relevant questions for the end. Assessment Initial assessment can be divided into three phases, these are: Primary Survey Resuscitation Phase Secondary Survey
Primary Survey
The primary survey is a rapid initial assessment the goal of which is to rapidly identify and manage injuries that pose an immediate threat to the patients life namely: Airway obstruction Chest injuries with compromise of the breathing or circulation Severe internal or external haemorrhage A systematic approach is essential so that nothing is missed, hence the ABCDE approach: A - Airway maintenance with cervical spine control. B - Breathing and ventilation. C - Circulation with haemorrhage control. D - Disability: neurological status. E - Exposure of the patient for a full examination. Life threatening injuries are identified and managed simultaneously.
Initial Management
The management of the severely injured patient requires rapid identification of management priorities based on their injuries, their vital signs and their mechanism of injury. A brief review of the steps involved in reception of severely injured follows:
Triage
This process is a distribution of resources to achieve the greatest good for the largest number of casualties. If the resources are sufficient the patients with life-threatening or multiple injuries are treated first. However if the number of casualties exceeds the capacity of the facility or staff then those casualties with the greatest chance of survival with the least expenditure of time, equipment and staff are managed first.
Airway (& Cervical Spine)

Assess the airway can the patient talk and breath freely? Is the airway obstructed or does it need to be protected ? Avoid the use of nasopharyngeal airways in the presence of head/facial trauma It is important to assume that in the presence of multiple trauma a cervical spine injury has occurred until ruled out by appropriate radiology and clinical examination.
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Pre hospital handover

The value of an accurate description of the environment and mechanism of injury cannot be overestimated. A brief summary of the mechanism of injury as well as pre-hospital
Trauma
Breathing
If oxygenation / ventilation is inadequate consider: Bag / mask ventilation Decompression of tension pneumothorax Drainage of haemothorax Closure of open pneumothorax
Resuscitation
Immediate resuscitation consists of management of hypovolaemia, oxygenation and haemorrhage control. During resuscitation continual re-evaluation of the ABCs is undertaken. At this stage urinary and nasogastric catheters can be inserted if indicated. Further monitoring including blood pressure, ECG and pulse oximetry will supplement the vital signs. Xrays of the lateral cervical spine, AP chest, and AP pelvis are useful early on, while films of other injuries can be delayed until after the secondary survey is complete. Blood is taken for cross match and investigations.
Circulation (& haemorrhage control)

Assess circulation. If inadequate then: Control external haemorrhage Establish at least two large bore peripheral IV cannulae ( 14 or 16G ) Cross match 6 units of red cells and consider need for FFP and platelets Rapidly administer 2 litres Hartmanns solution and assess response. In severe injuries, or if the patient must be transported, consider early placement of an arterial line. Consider the early use of O negative blood clotting factors or activated factor VII (Novoseven) if available (see below)
Secondary Survey
Systematic evaluation of the patient including history and physical examination The secondary survey is only undertaken when the primary survey is completed, resuscitation is well under way and the patients vital signs are normalizing. Consequently the secondary survey may well be delayed for up to several hours if the patient requires surgery or intervention to stabilize them.
Disability
Rapid assessment of level consciousness using the AVPU score: A awake V responding to verbal commands P responding to painful stimuli U unresponsive of
History
The AMPLE mnemonic suggested in the EMST course provides a useful summary of the patients history: A M P L E Allergies Current Medications Past medical history / Pregnancy Last meal Events / Environment relating to injury
Score of P or U corresponds to a GCS of 8 or less and suggests a need for airway protection. Assess pupils for symmetry
Exposure
The patient should be completely undressed and an active search made for significant injuries. Despite the need for a full examination it is important to avoid hypothermia in the trauma patient. Hypothermia is associated with poorer outcomes, and after examination the patient should be covered by warmed blankets of a forced air warming device.
Physical examination
Head Scalp Ocular examination Ear and tympanic membrane Periorbital soft tissue injuries Faciomaxillary injuries Neck Assume cervical injury in all patients Tracheal deviation Subcutaneous emphysema Neck veins Penetrating wounds
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Trauma
Chest Clavicles, ribs, sternum Heart and breath sounds Review chest Xray, preferably with a trauma surgeon or emergency physician Abdomen Bruising, tenderness Pelvis Avoid excessive manipulation of pelvic fracture Rectal / Vaginal examination Pregnancy test if appropriate Consider need for FAST scan Musculoskeletal Fractures and distal neurovascular deficits Peripheral pulses Spine and back (log-roll ) Wounds and other minor injuries Neurologic Assess GCS Pupils Spinal cord function Motor Sensory / reflexes The need for further investigations will be determined as a result of this review. However they may need to be delayed until initial, urgent surgical procedures have been undertaken. Determining the relative priorities for operative treatment, detailed radiological investigations, and transfer to other areas for definitive care requires collaboration and input from all senior staff managing the patient. These procedures should not interrupt the ongoing resuscitation and continuous reevaluation of the patient.
During such hand-over the essential elements of care need to be discussed while the notes and patient are examined. These are: History: Allergies, Medications, Past medical, Last meal, Environment of injury. Injury catalogue and active problem list. Treatments already undertaken [especially fluids administered] and response. Investigations undertaken and results available or pending. Blood products available. Surgical priorities, planning and coordination. An oral summary and completed documentation are both critical to preventing further injury to the patient.
Management of Large-volume Resuscitation

Resuscitation end-points
Traditionally, adequacy of fluid resuscitation is assessed by normalisation of blood pressure, heart rate and urine output. Suboptimal tissue perfusion persists, however, in a significant number of patients with multi-system trauma after normalization of blood pressure, heart rate and urine output . A number of alternate endpoints have been studied, the most practical being serum lactate, base deficit and gastric mucosal pH levels. There is evidence to suggest that normalization of one or all of these parameters as early as possible within the first 24 hrs following injury significantly improves survival in severely injured patients. Despite this, fluid resuscitation should not in any circumstances prevent the definitive treatment of injuries. Large volume resuscitation in trauma Patients who are hypovolaemic (more than 50% blood loss) following severe trauma are at high risk of developing multiple organ system failure and death The triad of acidosis, coagulopathy and hypothermia are associated with significantly increased mortality in this patient subgroup. Furthermore aggressive attempts to normalize haemodynamic parameters prior to control of hemorrhage have been shown to worsen outcome, particularly in penetrating trauma to the torso. Whilst the optimal algorithms for fluid
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Evolving Injuries
The early response to injury is a dynamic process. Continual review of the patients general condition is essential. Ongoing concealed blood loss can occur particularly with pelvic fractures. Acute brain swelling can diminish potential for long-term neurological recovery.
Hand-over of Care
Multiple transfers of management occur for the trauma patient. In-hospital transfers can involve both resuscitation teams [emergency medicine, anaesthetic, intensive care] as well as subspecialty surgical teams.
Trauma
resuscitation, blood product replacement, and the use of inotropes and/or vasopressor are yet to be determined, evidence suggests that resuscitation of the shocked trauma patient should be thought of in two phases. Initial resuscitation prior to control of hemorrhage should be limited to keep blood pressure around 90mmHg. Subsequent resuscitation focuses on the rapid surgical control of bleeding, by packing if necessary, aggressive reversal of acidosis, hypothermia and coagulopathy sometimes in the intensive care unit followed by delayed definitive repair of non bleeding injuries. There is evidence that crystalloid solutions may potentiate cellular injury caused by hemorrhagic shock and therefore blood products should be commenced earlier than normal. Fresh frozen plasma (FFP) should be ordered if the initial request of blood is 6 units or clinical impression of 50% blood loss. Ketchum suggests FFP before 1 blood volume is lost. Platelet requirements are less predictable but should be given after 10 units packed cells or earlier. Hb and clotting should be checked regularly. Cryoprecipitate and recombinant fVIIa may be required to correct refractory coagulopathy. Anecdotal evidence from the military suggests that early aggressive correction of acidosis and coagulopathy with minimal use of crystalloid significantly improves the outcome in casualties requiring major resuscitation.
disruption and/or obstruction. Diagnosis requires a high index of suspicion. Patients may be asymptomatic for 24-48 hours, and may have distracting injuries. High risk mechanisms include: Direct anterior neck trauma Steering wheel or dashboard in MVA (motor vehicle accidents) Clothes-lining injuries in motorcycle or bicycle accidents Other direct blows to the neck Severe Flexion / extension injuries Crush injuries e.g. attempted hanging Mechanism may predict site of injury Direct blow Laryngeal or cricoid cartilage injury more likely. Thyroid cartilage comminuted fractures causes separation of epiglottis from larynx Fractures of lateral portion of thyroid cartilage may cause false passages and fragments may obstruct intubation attempts. Extension / flexion injuries Tracheal tears or laryngotracheal separation may occur. Most commonly occurs at cricotracheal junction where connective tissue is weak. Airway held in close approximation by peritracheal tissue & strap muscles during negative pressure ventilation. Severed ends may be dislodged on attempts to pass an ETT.
Anaesthetic Implications of Airway Trauma

Blunt laryngeal trauma
Mortality rates of all airway injuries vary, but may range between 15-40%. Death is usually the result of associated injuries including aspiration (blood & recurrent laryngeal nerve injury), intrapulmonary haemorrhage, frank airway disruption and laryngospasm. Intubation may cause further trauma and failed attempts may precipitate complete airway
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Major diagnostic criteria suggestive of significant airway injury include: Dyspnoea Subcutaneous emphysema, Stridor, Inability to tolerate the supine position. The presence of major criteria has been suggested by some as an indication for immediate surgical tracheostomy under local anaesthesia Minor criteria include: Local swelling & tenderness Hoarseness, Dysphagia Haemoptysis.
Trauma
Assessment Investigations: Computed Tomography (CT). Regarded as investigation of choice by many, assesses integrity of larynx, condition of cricoarytenoid joints & endolaryngeal tissue not seen on fibreoptic endoscopy however CT is inadvisable in the presence of a major diagnostic feature. Laryngoscopy. Direct flexible nasolaryngoscopy/bronchoscopy is most well tolerated; it allows evaluation of cord movement, laryngeal mucosa & airway lumen with less risk of worsening cervical spine injury. Bronchoscopy may allow securing of the airway more distal to the injury, or endobronchial intubation if necessary. Use topical local anaesthetic with caution due to risk of aspiration. Indirect laryngoscopy may cause coughing / gagging & further compromise the airway. Cervical spine and chest X-rays may show subcutaneous (in particular cervical emphysema) & extrapleural air (pneumothorax or pneumomediastinum) & other associated injuries. Airway management Management should be considered case by case, is dependent likely injury and the skills of the managing team. If one or more major diagnostic feature is present, management should proceed in theatre with surgical assistance immediately available Options are: Endotracheal intubation under general anaesthesia use of an ETT at least one size smaller than usual has been suggested, uncut. Inhalational induction avoids use of positive pressure ventilation but there is the risk of aspiration in the [non-fasted] trauma patient. Intravenous induction may be necessary in the confused / uncooperative patient. Awake fibreoptic intubation Rigid laryngoscopy & bronchoscopy may allow intubation distal to the site of injury NB: Blind nasal intubation & percutaneous tracheostomy may exacerbate injury & are not advised.
Be aware: Cricoid pressure may dislocate fractured cricoid cartilage or entirely disrupt a partial tracheal transection. Positive pressure ventilation can exacerbate air leaks & worsen air dissecting around structures / surgical emphysema. Creation of false passages can occur during intubation attempts. Failed attempts at passage of ETT through a fractured portion may cause complete dislocation and obstruction Cricothyroidotomy may be useless in cricoid cartilage or distal trachea injury.
Airway burns
Most deaths from burns are secondary to respiratory complications mainly due to inhalation of toxic products of combustion. The injury of most concern in the acute management of trauma is that of thermal injury to the upper airway resulting in rapidly progressive oedema and obstruction. Signs suggestive of inhalational burns: Major Hoarse voice Brassy productive cough Stridor Facial, oral pharyngeal burns / oedema of face & mouth Minor Singed nasal hairs Carbonaceous sputum or oropharyngeal carbon Flash burns may cause superficial burns to face and lips and do not usually cause an upper airway burn, however the patient should still be assessed for the above signs. Management Major signs are highly suggestive of laryngeal injury and early intubation must be considered. Although maximal swelling usually occurs 1236 hours after injury, pharyngeal and laryngeal oedema may develop rapidly (over minutes) following inhalational burns to cause complete airway obstruction. Orotracheal intubation may rapidly become impossible, necessitating a surgical approach through a now anatomically distorted airway.
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Trauma
Be Aware: Inhalational injury may be associated with carbon monoxide poisoning. Burns are associated with drug or alcohol intoxication or psychiatric disturbance. Subsequent oedema may be extensive so an uncut endotracheal tube should be used.
Emergency department thoracotomy (EDT) is a drastic procedure with limited utility. It should be reserved for patients who are in extremis following penetrating trauma to the chest where pericardial tamponade is suspected and appropriate surgical expertise is immediately available.
Intra-cranial Trauma Anaesthetic Implications of Chest Trauma

Major chest trauma is usually fatal on scene so the survivors reaching hospital are a selfselecting group. Only 15% of them require an operation. The rest may need volume replacement, ventilation, chest drains and analgesia. The chest Xray is an essential and vital source of information and needs to be carefully and systematically evaluated. Major airway injury is suspected when there is surgical emphysema in the neck, mediastinal air or pneumopericardium on the CXR. If it is suspected, attempt to delay intubation and IPPV until bronchoscoped. Chest drains should only precede the CXR if the patient is deteriorating rapidly. Chest tube insertion should be performed by surgical incision followed by blunt plural dissection. Use of the trochar when inserting the tube is NOT recommended due to the increased incidence of lung damage with this method. Keeping the pleural cavity empty will help to seal off air leaks and stop bleeding. Thoracotomy is not usually needed unless the blood loss is more than 1500 mls initially or more then 200 mls/ hour for two hours.' A larger volume of blood than this suggests the injury is not just one or two intercostals vessels but potentially something more significant. Cardiac tamponade most commonly results from cardiac laceration following a penetrating wound. It is characterised by distended neck veins (may not be present in a hypovolaemic patient), hypotension and muffled heart sounds. The diagnosis may be confirmed on FAST ultrasound. Pericardiocentisis is of little use as the blood in the pericardium is usually clotted and may result in laceration of the ventricle or coronary arteries. Urgent transfer to theatre for thoracotomy is the management of choice.
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About 50% of trauma deaths are associated with Traumatic Brain Injury (TBI). Early management of TBI should be direct toward minimizing progression of injury in the at risk brain. Specific aims for the anaesthetist are: Minimise secondary insults. Detect neurological deterioration during management of other injuries. Seek neurosurgical advice to aid effective decision-making. Undertake specific neuro-resuscitative measures when required. Secondary injury can result from a number of causes with specific management requirements: Hypotension is strongly associated with poor outcome in TBI. A number of studies suggest that a single systolic pressure below 90mmHg is associated with a two to three-fold increases in. Hypoxia hyper/hypocapnoea and hyper/ hypoglycemia are also associated with poor outcome, however the evidence is less definitive.
Management strategies for TBI

Fluid resuscitation Given the strong association between hypotension and poor outcome, the systolic blood pressure should be maintained above 90mmHg, although different groups recommend higher pressures. The theoretical risk of large volumes of fluid worsening cerebral oedema does not seen to be supported in clinical practice, although there may be some benefit in use of hypertonic saline in TBI. There is insufficient evidence to support use of one vasoactive agent above another if fluids alone are insufficient to maintain arterial pressure.
Trauma
Coagulopathy may increase intracranial bleeding, so should be aggressively managed. Ventilatory control Hypoxia, hypo- and hyper capnoea are all viewed as avoidable secondary insults. SpO2 should be maintained above 90% and PaCO2 between 35-40 mmHg. Patients with GCS of <9, who are unable to maintain their own airway or respiratory parameters or who are requiring CT scanning or other investigation / intervention are candidates for intubation and controlled ventilation. Glycaemic control Hypoglycemia should be corrected and hypoglycemia avoided, but optimum targets are yet to be defined. Transfer The presence of a significant TBI will generally require management in a center with appropriate expertise. In peripheral centres management should be directed at stabilization and early transfer. Monitoring During prolonged procedures to treat other injuries to the trunk or limbs it is important to monitor for deterioration. This may require placement of an ICP [intracranial pressure] monitor by a neurosurgeon. Specific neuro-resuscitative measures can temporarily delay the effect of a rising ICP. Head up positioning [20 degrees] and adequate muscle relaxation optimise cerebral venous pressure. Mannitol infusion [0.5 1 gram/ kg] and acute hyperventilation may also be indicated in some situations to provide a shortterm reduction in ICP. The use of urgent decompressive craniotomy for raised ICP due to closed head injury is becoming more common, and may become the standard of care.
Although the usefulness of the lateral cervical spine film has recently been questioned. These X-rays: are performed as part of the secondary survey should not prevent resuscitation efforts preferably be done in the resuscitation area of A&E (radiology departments are often not equipped for ongoing resuscitation) should be referred for specialist radiological opinion if any doubt remains as to the presence of pathology Clearing the cervical spine The diagnosis of an unstable spinal injury and its subsequent management can be difficult, and a missed spine injury can have devastating long-term consequences. In trauma patients therefore, spinal column injury must therefore be presumed until it is excluded. Clearance of the cervical spine in trauma patients is one of the most contentious issues in trauma care and should not be the sole responsibility of the anaesthetist. In the acute phase of trauma management, the focus should be on appropriate spinal immobilsation, rather than spinal clearance. Imaging of the spine should not take precedence over lifesaving therapeutic and diagnostic procedures. Initially a rigid cervical immobilisation collar should be used, however these are likely to cause pressure related injuries, so should be changed to the more anatomically correct Philadelphia collar as soon as possible, preferably within four hours. The Cervical spine may be clinically cleared in hospitalized patients if the following conditions are met: Normal alertness No drug or alcohol impairment No midline cervical tenderness No focal neurologic deficit No significant distracting injury Pain free range of active movements If these conditions are not met, then cervical spine immobilization is indicated until the neck can be cleared by radiological evaluation. Guidelines and protocols vary between institutions depending on expertise and facilities available, and may include CT scan and / or MRI. Practitioners should familiarize themselves
77
X-Rays in the Trauma Setting

General It is regarded as standard practice that three standard X-rays are taken in the multi-trauma patient. 1. Lateral cervical spine 2. Chest 3. Pelvis
Trauma
with guidelines relevant to their own institution, however general guidelines are available in the bibliography section Viewing of X-Rays There are many different approaches to viewing X-rays which may be valid. Experienced clinicians use their own approach. However the following is just one such approach. X-rays should always be examined on a viewing box or computer screen and the following features should be sought: 1. Correct orientation of film or view. 2. Name of the Patient 3. Date of the film These factors, often overlooked in the busy resuscitation period, are important as often multiple patients X-rays are viewed at the same box. Following on from this The ABC approach can be used. 1. Adequacy of the X-ray: Technical factors: adequate penetration of the film Patient factors: are all the anatomical features included. 2. Bones: Look for any lucency to indicate fractures by carefully following the outline of each bone (e.g. rib or vertebrae) Look for fragments of bone. Look for alignment of bones (particularly important in the C-spine) 3. Cpaces and other soft tissues: 4. Diaphragm and Disc spaces in the CXR and C-spine respectively. 5. Extras: This refers to additional equipment often placed in the patient such as nasogastric and endotracheal tubes. Lateral Cervical Spine If there remains any clinical doubt re the stability of the C-spine expert radiological/neurosurgical or orthopaedic advice should be sought. Until such time the patient should be treated as an unstable spine with appropriate immobilisation. A normal lateral C-spine film may also miss up to 15% of injuries. Children may also sustain significant cord injury without any bony injury. The following features are sought. 1. Adequacy: The lower part of the skull, all seven
78
cervical and the first thoracic vertebrae must be seen. The x-ray should be of reasonable penetration such that the bony and soft tissues are clearly visible. It should be taken in the neutral plane. 2. Bones: Correct alignment of the bones is assessed by tracing four lines: Anterior vertebral bodies Anterior spinal canal (or posterior vertebral bodies) Posterior spinal canal Spinous process tips These lines should trace a gentle continuous curve and any deviation >3 mm would indicate a dislocation. Vertebral bodies: anterior height should not be <3mm posterior height The distance between the anterior arch of C1 and the odontoid peg should be < 3 mm. 3. Cpaces and soft tissues: The prevertebral soft tissues should be <5 mm. Any widening of this space would tend to indicate a fracture or dislocation. The interspinous ligaments should be inspected for any widening indicating a dislocation 4. Discs: Intervertebral discs and facet joints should be examined 5. Extras: Look for bony fragments in the spinal canal. Check path of nasogastric and endotracheal tubes. Chest X-ray Look for the following features: 1. Adequacy: Penetration of the film should such that the disc spaces of the lower vertebrae can be seen through the cardiac shadow. The entire chest wall and both costophrenic angles should be visualised. Rotation of the film can be assessed by comparing the distance between the clavicles and the spinous processes. In the trauma setting often an AP rather than a standard PA film is obtained. 2. Bones: Initially the humerus, clavicles and scapula on both sides are inspected. Thereafter the ribs on each hemi-thorax are
Trauma
individually traced looking for fractures. Fractures of the upper three ribs are associated with cardiac, aortic and bronchial injury. Rib fractures are associated with a haemothorax and pneumothorax. Lastly the vertebrae are inspected. 3. Cpaces and soft tissues The mediastinal structures are examined from top to bottom The trachea should be centrally placed. In a child the thymus may give an appearance of a widened mediastinum. The aortic arch should be uniform and clear. Widening of the mediastinum may indicate a traumatic rupture of the aorta. The cardiac shadow should lie 2/3 in the left hemi-thorax. AP films tend to exaggerate the size of the heart. Displacement of the heart is either due to the mediastinum being pushed across (e.g. tension pneumothorax) or being pulled (e.g. collapse of a lung). A globular shaped cardiac shadow may indicate a haemopericardium or pericardial effusion. The lung fields should be individually assessed and then compared to each other. Lung markings must be seen to the edge of the lung fields. The soft tissues surrounding the chest may contain foreign bodies or subcutaneous air indicating a pneumothorax. 4. Diaphragm: The right diaphragm is normally situated above the left. Blunting of the costo-phrenic angles may indicate a haemothorax, pleural effusion or diaphragm rupture. The appearance of stomach or small bowel in the chest indicates diaphragm rupture. 5. Extras: Endotracheal tube should be placed in the trachea above the carina. Nasogastric tubes in the left hemithorax indicate a ruptured diaphragm. ECG leads and intercostal drains may be seen.
ABC of Major Trauma. Skinner D, Driscoll P, (Eds) BMJ Publishing (3rd ed. 1999). Textbook of Adult Emergency Medicine. Cameron P (Ed) Churchill Livingstone (2000).
Websites
Liverpool Hospital Trauma Services Department website - www.swsahs.nsw.gov.au/livtrauma www.trauma.org Excellent image bank and range of teaching resources. Range of guidelines esp clearing the cervical spine. Good links to other trauma related websites www.east.org/tpg Wide range of trauma practice guidelines
Cervical spine
www.trauma.org - Articles / Hoffman JR, Mower WR, Wolfson AB, Todd KH, et al. NEJM. Jul 13,2000. 343(2):94-100
Resuscitation
Holcomb JB et al. Damage control resuscitation: Directly addressing the early coagulopathy of trauma. J Trauma. 2007;62:307310. Tisherman SA et al .Clinical Practice Guideline: Endpoints of resuscitation. J Trauma. 2004;57:898912. Ketchum L, Hess JR, Hiipala S. Indications for early fresh frozen plasma, cryoprecipitate and platelet transfusion in trauma. J Trauma. 2006;60:S51S58 Porter JM, Ivatury RR. In search of optimal endpoints of resuscitation in Trauma patients: a review. J Trauma. 1998: 44: 908-914. Cotton BA.The cellular metabolic and systemic consequences of aggressive fluid resuscitation strategies. Shock. 2006; 26: 115-121. Holcomb JB. Use of recombinant activated factor VII to treat the acquired coagulopathy of trauma. J Trauma. 2005;58:1298 1303
Airway Trauma
Hurford WE, Peralta R. Management of tracheal trauma. Canadian Journal of Anesthesia. 2003;50:R4 Pancholi SS. Laryngeal Fractures. http://www.emedicine.com/ent/topic488.htm Ma S, Christey G. Case report Non-operative management of a blunt hypopharyngeal injury. Liverpool Hospital Trauma Services Department website, Available online 18 January 2006. www.swsahs.nsw.gov.au/livtrauma Miller K, Chang A. Acute inhalation injury. Emerg Med Clin N Am. 2003;21:533-557. Garner JP, Jenner J, Parkhouse DAF. Prediction of upper airway closure in inhalational injury. Military Medicine. 2005;170: 677-682.
Further Reading General

ATLS: Advanced Trauma Life Support Program for Doctors. American College of Surgeons Committee on Trauma. (1994)
79
Trauma
Thoracic trauma
Meredith JW, Hoth JJ. Thoracic trauma: when and how to intervene. Surg Clin N Am. 2007;7:95118.
Neurotrauma
Moppett IK. Traumatic brain injury: assessment resuscitation and early mamgement.Br J Anaesth. 2007;99:18-31.
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EMAC Participants Manual 2010-1

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EMAC Participants Manual 2010-1

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EFFECTIVE MANAGEMENT OF ANAESTHETIC CRISES

AUSTRALIAN AND NEW ZEALAND COLLEGE OF ANAESTHETISTS

Introduction to First Edition

Introduction to Second Edition

Human Performance Issues

Human Performance Issues

Human Performance Issues

Human Performance Issues

Human Performance Issues

Human Performance Issues

Generic Principles for Prevention & Management of Difficult Clinical Situations

1. Know, Modify & Optimise Your Environment

2. Anticipate & Plan

Human Performance Issues

5. Call for Help or a Second Opinion Early Enough

3. Ensure Leadership and Role Clarity

Human Performance Issues

7. Distribute the Workload & Use All Available Resources

Human Performance Issues

Performance-Shaping Factors, Including Production Pressure

Human Performance Issues

Fatigue and Sleep Loss

Human Performance Issues

Human Performance Issues

Other Performance-shaping Factors

Human Performance Issues

Teamwork Issues: Social Psychology of the Operating Theatre

Systems Approach to Patient Safety

Human Performance Issues

Human Performance Issues

Suggested Further Reading:

Demand Wall tension 3 Heart rate Contractility

Myocardial Ischaemia & Acute Coronary Syndromes

Coronary blood flow Arterial oxygen content

Management of Acute Myocardial Ischaemia

Myocardial Oxygen Supply and Demand

ST segment changes of 1-2mm T wave inversion Arrhythmias

Platelet Inhibitors and anti-coagulants

Thienopyridine ADP Receptor antagoninsts (e.g. clopidogrel)

Glycoprotein IIb/IIIa inhibitor (e.g. Abciximab)

The Acute Coronary Syndromes [2]

Diagnosis of Acute Coronary Syndrome due to Coronary Artery Disease

Cardiac Arrest & Post-Arrest Care

Unmonitored in-hospital cardiac arrest

Out-of-hospital cardiac arrest

Perioperative cardiac arrest

Management of Perioperative Cardiac Arrest [11] Declare a crisis

Universal ACLS Algorithm

Hunt for Ventricular Fibrillation or Ventricular Tachycardia

Search for cause (memorize 4 Hs and 4 Ts)

Post Resuscitation Care and Periarrest Conditions [7, 14]

Life Threatening Cardiac Rhythms [7]

Disorders of impulse conduction - blocked or re-entrant. Combinations of these.

Management of Cardiac Arrhythmias

Initial Therapy Most readily available of Electrical therapy - Pacing Drugs

Tachycardia Unstable but not immediately life threatening Tachycardia Bradycardia

Table 1. Simplified Approach to Dysrhythmias

Tachyarrhythmias [7, 17, 19]

Table 2. Simplified antiarrhythmic choices

Amiodarone Esmolol Digoxin

Energy (R=resistance and t=time) R.t

Table 3. Simplified first shock energy settings [6]

Crises with Valvular Heart Disease

myocardial ischaemia without having coronary artery disease.