emac participants manual 2010-1

EFFECTIVE

MANAGEMENT OF

ANAESTHETIC CRISES

PARTICIPANT MANUAL SECOND EDITION 2010

©ANZCA

iii

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

iv

Published in 2010 by

Australian and New Zealand College of Anaesthetists,

630 St Kilda Road

Melbourne Victoria 3004

Australia

v

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 GABA‟S 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

vi

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 individual’s 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

vii

Introduction to Second Edition The EMAC Course represents an on-going

endeavour by a group of medical and non-

medical 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 ANZCA’s 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

Human Performance Issues

1


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

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:

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.


2

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

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 Miller‟s 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


3

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

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 & re-

evaluation. Gaba describes the anaesthetist‟s

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 anaesthetist‟s

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 anaesthetist‟s own thought

processes. This ability to “think about one‟s

own thinking” in order to strategically control

one‟s 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 anaesthetist‟s

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


4

fact the anaesthetist‟s 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.

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 anaesthetist‟s 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

anaesthetist‟s 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 anaesthetist‟s

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 re-

evaluation 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.


5

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 end-

results 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 anaesthetist‟s

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

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.

Gaba’s Seven “Key Points” for Preventing & Managing Critical Events

Several basic principles may help manage a

crisis more effectively, especially as humans

aren‟t 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 al‟s crisis management


6

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.

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.

4. Communicate Effectively

Let others within the team know when a

“situation” is developing. Give clear specific

instructions to those you are managing. Don’t

be vague. Don’t 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.

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 don‟t wait too long to call.

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 individual‟s

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!

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

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

anaesthetist’s limited attention span.

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.

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”.

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

environment…the 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 environment…the comprehension

of their meaning and the projection of their status in the near future (Endsley, 1995).


8

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 operator‟s

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.

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 &

outcome.

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


9

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.

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

anaesthetist‟s responsibility to ensure they get

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 14:00-

18:00. 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


10

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

one‟s 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. One‟s 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

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

one‟s 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


11

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.

Other Performance-shaping Factors

There are a number of other performance-

shaping 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

anaesthetist‟s 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.

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)

These attitudes include:

"Don't tell me what to do.” (Anti-

authority) 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.

“I’ll 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

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 patient‟s 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!


12

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 one‟s 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, lower-

status team-members tend to defer to a higher-

status 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

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 people‟s personalities can‟t be changed,

individual‟s 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

system‟s “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 system-

related 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 time-

compressed, corridor pre-operative

assessment. In discussing this case the

systems approach asks: “How can we

change the system to prevent this


13

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.

Don‟t 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.

Don‟t be satisfied with explanations such

as “That‟s the way the system is and

there‟s 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.

Operational procedures (e.g. “Time-

out”).

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


14

and manage all the crises that you face,

regardless of how they might be triggered.

Utilise your department‟s 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!

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 what‟s 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)

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. Flin RH, O'Connor P, Crichton M. Safety at

the sharp end. Aldershot: Ashgate; 2008.

2. Gaba DM, Fish KJ, Howard SK. Crisis

Management in Anesthesiology. New York:

Churchill Livingstone; 1994.

3. Rall M, Gaba D. Chapter 83. Human

Performance and Patient Safety. In: Miller's

Anesthesia. New York: Elsevier; 2005.

4. 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.

5. 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.

6. Lingard L. Perceptions of operating room

tension across professions: building

generalisable evidence and educational

resources. Academic Medicine 2005;80:S75-

9.

7. Reason J. Human error: models and

management. BMJ 2000;320:768-70.

8. Runciman W, Merry A, Walton M. Safety and

ethics in healthcare: a guide to getting it right.

Aldershot: Alshgate; 2007.

http://www.chfg.org.uk/

Cardiovascular Emergencies

15

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.

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

2 Thank to Drs Paul Dalley and Chris Horrocks for kindly

commenting on the draft version of this chapter.

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.


16

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.

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]

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.

Supply Demand

Coronary blood flow

Arterial oxygen content

Wall tension 3

Heart rate

Contractility

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 end-

diastolic 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 Increased Demand

Reduced Coronary Blood

Flow

Tachycardia

Hypotension

Elevated LVEDP Reduced Arterial Oxygen

Content

Anaemia

Hypoxaemia

Increased Wall

Tension

Hypertension

Hypervolaemia Increased Heart

Rate

Increased

Contractility

Symptoms in the conscious patient:

Chest pain

Sweating

Reversible ECG changes and haemodynamic

perturbations may be noted in anaesthetized

patients:

3

Wall Tension

Pressure Radius

2 Thickness


17

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 anti-

platelet 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

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 5-

10 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 anti-

platelet 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


18

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.

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 ST-

depression 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

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.


19

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 beta-

blockers. 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.

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.

Posterior infarction (ST depression in V1-

V4).

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.

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.


20

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-of-

hospital cardiac arrest.

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.

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 non-

arrhythmic 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].


21

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 non-

anaesthetised 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].

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 non-

shockable 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.

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 H‟s and

T‟s.

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


22

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 120-

200J, 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].

Search for cause (memorize 4 H’s and 4 T’s)

Hypovolaemia (the most common cause)

Hypoxaemia

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].:


23

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.


24

Post Resuscitation Care and Peri-arrest 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 long-

term, 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. Post-

arrest 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 post-

resuscitation 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 1-

year neurologic outcome [14].

Hyperventilation may worsen neurologic

outcome, and normocarbia is recommended.

Mild induced hypothermia (32°-34°C)

improves neurologic outcome among initially

comatose survivors, but its practical

application may be difficult. Patients should

not be rewarmed from mild spontaneous

hypothermia (>33°C), 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


25

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 life

threatening?

Does the patient need CPR?

Is the rhythm slow or fast?

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.

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 patient‟s

ECG may identify predisposing features.

Mechanisms of Cardiac Arrhythmia

Disorders of impulse generation -

increased or decreased.

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

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

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

Urgency Rhythm Initial Therapy

Life threatening

Bradycardia Most readily available of

Electrical therapy - Pacing

Drugs

Tachycardia Electrical therapy - Cardioversion

Unstable but not immediately

life threatening

Bradycardia Reverse cause

Consider drugs

Tachycardia Reverse cause

Consider drugs


26

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 β-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


27

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

than 2 days, the immediate goal is rate

control, with consideration of anti-

coagulation 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.


28

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 120-

150J

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

Narrow-Complex

Tachycardia

Atrial Fibrillation

First

Choice

Amiodarone Adenosine for SVT Esmolol for rate

Amiodarone or

Flecainide for rhythm

Second

Choice

Lignocaine Amiodarone Esmolol

Digoxin

Ca++-blocker,

amiodarone or

digoxin for rate

Table 2. Simplified antiarrhythmic choices

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 re-

entry. 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


29

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 re-

entrant 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 non-

synchronised shock. Unsynchronized

mode is usually the default setting.


30

CurrentEnergy

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

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 manufacturer-

specific. 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

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

Narrow-Complex or

Atrial Flutter

Biphasic 120-150 J 70-120 J

Monophasic 200 J 100 J

Table 3. Simplified first shock energy settings [6]


31

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.


32

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].

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 β-

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 α-

agonist. Patients with aortic stenosis or

hypertrophic cardiomyopathy may develop

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.

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.


33

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 β-blockade.

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. 180-

209/110-119) 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 μg/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

administered. Caution should be exercised

if administering β-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.

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


34

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. Poisseulle‟s 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)

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

feasible…similar to a 20-22 gauge IV, but

a small IV is better than no IV.

http://www.facs.org/trauma/publications/vasaccess.pdf

http://www.facs.org/trauma/publications/vasaccess.pdf


35

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.

2. 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.

3. Antman, E.M., et al., 2007 Focused

Update of the ACC/AHA 2004 Guidelines

for the Management of Patients With ST-

Elevation Myocardial Infarction.

Circulation, 2008. 117(2): p. 296-329.

4. 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.

5. Morley, P., Adult Cardiopulmonary

Resuscitation in 2007, in Australasian

Anaesthesia 2007, R. Riley, Editor. 2007,

ANZCA: Melbourne. p. 9-17.

6. 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.

7. Nolan, J.P., et al., European Resuscitation

Council guidelines for resuscitation 2005.

Section 4. Adult advanced life support.

Resuscitation, 2005. 67 Suppl 1: p. S39-

86.

8. 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.

9. 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.

10. 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.

11. Runciman, W.B., et al., Crisis

management during anaesthesia: cardiac

arrest. Qual Saf Health Care, 2005. 14(3):

p. e14.

12. ILCOR, 2005 International Consensus on


Emergency Cardiovascular Care Science

with Treatment Recommendations. Part 2:

Adult basic life support. Resuscitation,

2005. 67(2-3): p. 187-201.

13. 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.





Postresuscitation Support. Circulation,

2005. 112(24): p. IV-84-IV-88.

15. Morris, R.W., et al., Crisis management

during anaesthesia: hypotension. Qual Saf

Health Care, 2005. 14(3): p. e11.

16. Atlee, J.L., Perioperative cardiac

dysrhythmias: diagnosis and management.

Anesthesiology, 1997. 86(6): p. 1397-424.

17. Thompson, A. and J.R. Balser,

Perioperative cardiac arrhythmias. Br J

Anaesth, 2004. 93(1): p. 86-94.




Emergency Cardiovascular Care Part 5:

Electical Therapies. Circulation, 2005.

112(24): p. IV-35-IV-46.





Management of Symptomatic Bradycardia

and Tachycardia. Circulation, 2005.

112(24): p. IV-67-IV-77.

20. Fuster, V., et al., ACC/AHA/ESC 2006

Guidelines for the Management of Patients

with Atrial Fibrillation. Circulation, 2006.

114(7): p. e257-354.

21. 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.

22. Sulke, N., F. Sayers, and G.Y. Lip,

Rhythm control and cardioversion. Heart,

2007. 93(1): p. 29-34.

23. Kalra, L. and G.Y. Lip, Antithrombotic

treatment in atrial fibrillation. Heart,

2007. 93(1): p. 39-44.

24. Delacretaz, E., Clinical practice.

Supraventricular tachycardia. N Engl J

Med, 2006. 354(10): p. 1039-51.

25. Salukhe, T.V., D. Dob, and R. Sutton,

Pacemakers and defibrillators:

anaesthetic implications. Br J Anaesth,

2004. 93(1): p. 95-104.

26. 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.


36

27. 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.

28. Poliac, L.C., M.E. Barron, and B.J. Maron,

Hypertrophic cardiomyopathy.

Anesthesiology, 2006. 104(1): p. 183-92.

29. 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.

30. Paix, A.D., et al., Crisis management

during anaesthesia: hypertension. Qual

Saf Health Care, 2005. 14(3): p. e12.

31. Allman, K.G., A.K. McIndoe, and I.H.

Wilson, eds. Emergencies in Anaesthesia.

2005, Oxford University Press: Oxford.

32. Selim, M., Perioperative stroke. N Engl J

Med, 2007. 356(7): p. 706-13.




Emergency Cardiovascular Care Part 9:

Adult Stroke. Circulation, 2005. 112(24):

p. IV-111-IV-120.

34. Singleton, R.J., et al., Crisis management

during anaesthesia: vascular access

problems. Qual Saf Health Care, 2005.

14(3): p. e20.

35. Miller, L., G.C. Kramer, and S. Bolleter,

Rescue access made easy. Journal of

Emergency Medical Services 2005.

30(10): p. suppl 8-18.

36. Schwartz, D., et al., The use of a powered

device for intraosseous drug and fluid

administration in a national EMS: a 4-

year experience. J Trauma, 2008. 64(3): p.

650-4; discussion 654-5.

37. 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.

http://www.scopus.com.wmezproxy.wnmeds.ac.nz/scopus/source/sourceInfo.url?sourceId=35652

Airway Emergencies

37

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

patient’s 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 over-

reliance upon instinctive pattern recognition

and problem solving may contribute to sub-

optimal 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.

Airway Emergencies

38

The Primary Plan For Airway Management

Your preferred approach to a case is your

primary plan. It reflects best practice tailored

to the individual patient‟s needs, intended

surgery and operating environment. A

decision-support tool is shown in Box 1.

1. Assess your patient and situation

2. Analyse your options in terms of risks and

benefits

3. Make a provisional plan

4. Road-test this with medical and nursing

colleagues

5. Revise if necessary

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 Lehane‟s grading of the view obtained

during direct larygoscopy5 (figure 1 (b)).

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).

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

Anaesthetist‟s 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.

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 co-

workers7 (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

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.

Problem Incidence (%)

Intubation requiring several attempts or

different blades

1-18

Intubation possible, but Cormack and

Lehane Grade IV

1-4

Intubation impossible 0.05-0.35

Intubation and ventilation impossible

leading to cerebral damage

0.0001-0.02

Airway Emergencies

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

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 laryngoscope‟s 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

“can‟t intubate, can‟t ventilate” situation.

Assessment of the airway in the supine

position is useful in these patients.

Airway Emergencies

40

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).

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?

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

Resources

Environment

Surgery

Patient

Airway Risks

You

Airway Emergencies

41

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 designer‟s 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 know-

how 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.

Airway Emergencies

42

Figure 4: Basic structure of DAS unanticipated difficult intubation flow-chart.

Airway Emergencies

43

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

1 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

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.

2 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

.

3 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

.

4 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.

5 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

Airway Emergencies

44

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 “can‟t intubate - can

ventilate” situation to a “can‟t intubate,

can’t 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

“can‟t intubate, can‟t ventilate” situation.

These include cannula cricothyroidotomy and

the emergency surgical airway. The time-

critical, “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

Airway Emergencies

45

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 “Can‟t intubate -

Can‟t 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.

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

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 Sedated or comatose

(sedation, narcotisation,

coma)

Snoring, periodic

breathing

Anatomical Obstruction

(post surgical swelling,) Patient alert,sits forward

haematoma, foreign body,

traumatised larynx)

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

Airway Emergencies

46

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.

Airway Emergencies

47

Figure 5. DAS Flow-chart for ”can‟t intubate, can‟t ventilate” situation.

Airway Emergencies

48

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 purpose-

designed 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

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

49

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.

The patient‟s 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

Box 4: Recognition of Compromised Breathing or

Ventilation

Look, Listen & Feel

for:

Consider patient unstable

if*:

Ventilatory drive Respiratory rate <5 or

>36 bpm

Increased work of

breathing

Use of accessory muscles

Abnormal breath sounds 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

Airway Emergencies

50

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 non-

invasive pressure support via a purpose-

designed 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 to

manage severe bronchconstriction.

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 anaesthetist‟s performance,

and that of the team. In retrospect, the patient

will be viewed to have received appropriate

care, irrespective of the outcome.

Airway Emergencies

51

Appendix 1 : Difficult Airway Society Algorithms

Airway Emergencies

52

Airway Emergencies

53

Airway Emergencies

54

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

patient‟s 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 scalpel-

made 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

patient‟s circumstances, the operator‟s

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.

Airway Emergencies

55

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

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

56

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.

2. Howard SK, Gaba DM. Factors

influencing vigilance and performance of

anesthetists. Current Opinion in

Anesthesiology 1998: 11: 651-57.

3. Weingart SN, Wilson RMcL, Gibberd

RW, Harrison B. Epidemiology of

Medical Error. BMJ 2000;320:774-7.

4. Cheney FW, Posner KL, Lee LA, Caplan

RA, Domino KB. Trends in Anesthesia-

related Death and Brain Damage: A

Closed Claims Analysis. Anesthesiology

2006: 105; 1081-6

5. Cormack RS and Lehane J. Difficult

tracheal intubation in obstetrics.

Anaesthesia 1984

6. Crosby ET, Cooper RM, Douglas MJ et al.

The unanticipated difficult airway with

recommendations for management. Can J

Anaesth. 1998. 45; 7: 757-76.

7. Cooper SD, Benumof JL. Airway

Algorithm: Safety Considerations. Chapter

9 in Patient Safety in Anesthetic Practice.

RC Morrell (ED). Churchill Livingstone

1997

8. Janssens M and Hartstein G. Management

of the difficult intubation. European

Journal of Anesthesiology 2001: 18: 3-12.

9. Savva D. Prediction of difficult tracheal

intubation. Brit J Anaesth, 1994; 73: 149-

153

10. Rose DK, Cohen MM. The airway:

problems and predictions in 18,5000

patients. Can J Anaesth 1994: 41: 372-83.

11. Benumof JL. Definition and Incidence of

the Difficult Airway in: Benumof JL, ed.

Airway Management: Principles and

Practice. Philadelphia, USA: Mosby,

1995: 121-5.

12. Lyons G. Failed intubation: six years

experience in a teaching maternity unit.

Anaesthesia 1985: 40: 759-62.

13. Tsen LC, Pittner R, Camann WR. General

anaesthesia for caesarean section at a

tertiary care hospital 1990-95: indications

and implications. International Journal of

Obstetric Anaesthesia 1998: 7: 147-52.

14. Hawkins JL, Gibbs CP. General

anaesthesia for caesarean section: are we

really prepared? International Journal of

Obstetric Anaesthesia 1998:7:145-46.

15. Hawkins JL, Koonin LM, Palmer SK,

Gibbs CP. Anesthesia related deaths

during obstetric delivery in the United

States. 1979-90. Anesthesiology

1997:86:277-84.

16. Keller C, Brimacombe J, Kleinsasser A,

Loeckinger A. Does the ProSeal laryngeal

mask airway prevent aspiration of

regurgitated fluid? Anesthesia and

Analgesia 2000; 91: 1017–20.

17. Brimacombe J, Keller C. Airway

protection with the ProSeal laryngeal mask

airway. Anaesthesia and Intensive Care

2001; 29: 288–91.

18. Evans NR, Gardner SV, James MF.

ProSeal laryngeal mask protects against

aspiration of fluid in the pharynx. British

Journal of Anaesthesia 2002; 88: 584–7.

19. Maltby JR, Beriault MT, Watson NC, Fick

GH. Gastric distension and ventilation

during laparoscopic cholecystectomy:

LMAClassic vs. tracheal intubation. Can J

Anaesth 2000; 47: 622-6

20. Ilzuka T, Kinoshita K, Fukui H.

Pulmonary compliance of the laryngeal

mask airway during laparoscopic

cholecystectomy. Anesth Analg 2000; 90:

52; 10.

21. Lu P.P, Brimacombe J, Yang C, Shyr M.

ProSeal versus the Classic laryngeal mask

airway for positive pressure ventilation

during laparoscopic cholecystectomy.Brit

J Anaes 2002:.88; 824-8

22. Caponas G. Intubating laryngeal mask

airway. Anaesthesia and Intensive Care

2002; 30: 551-69

23. Agro F, Brimacombe J, Brain AI,

Marchionni L, Cataldo R. The intubating

laryngeal mask for maxillofacial trauma.

European Journal of Anaesthesiology

1999; 16: 263–4.

Airway Emergencies

57

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: 1342–6.

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):1335-

42.

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:

136–40.

35. Knill RL. Difficult laryngoscopy made

easy with a „BURP‟. Canadian Journal of

Anaesthesia 1993; 40: 279–82.

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: 135–6.

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:

1269–77.

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: 1222–3.

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: 937–9.

48. Richards CF. Piriform sinus perforation

during Esophageal-Tracheal Combitube

placement. Journal of Emergency

Medicine 1998; 16: 37–9.

49. Vezina D, Lessard MR, Bussieres J,

Topping C, Trepanier CA. Complications

associated with the use of the Esophageal-

Tracheal Combitube. Canadian Journal of

Anaesthesia 1998; 45: 76–80.

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.

Airway Emergencies

58

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]

http://www.emedicine.com/med/topic2011.htm

http://www.emedicine.com/med/topic2011.htm

Airway Emergencies

59

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.

Anaesthetic Emergencies

60

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 doesn’t

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

Gaba’s “Initial Response to a Serious Event”

(Crisis Management in Anesthesiology, 4)

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?

4 Gaba DM, Fish KJ, Howard SK. Crisis Management in

Anesthesiology. New York: Churchill Livingstone; 1994.

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. It‟s a useful strategy to learn

the names of your team. Ensure your requests

have been acknowledged and accepted. Conflict

can arise. Focus on what‟s 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 team‟s activities. The leader

should have a global view of what‟s 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

doesn‟t 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 well-

rehearsed 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


61

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 you’ve

handed out the tasks, check that the team is

coping with the tasks they’ve 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. Don’t wait for

the next emergency or next EMAC course.

Practice them on a daily at work.

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 we’re not looking, we won’t 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?

Allocate attention wisely

We can only attend to a limited number of pieces

of information at once. It’s easy to overlook

something if we’re 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 you’re

thinking, what you’ve considered and what you

can’t work out. They are brought up to speed,

may see things you’ve missed or misinterpreted,

or come up with a new suggestion. Consider

what it’s like trying to help a junior doctor with

an endotracheal intubation if they don’t say what

they’re seeing, what problem they’re

encountering. It’s 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 you’ve missed.

Are certain ways of conveying the problem to

responders more useful than others? If, as a

helper, we’re 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


62

A Systematic Approach to Crisis Management

In a crisis, we need to gather all the relevant

information. Problems arise when we

overlook important information. It’s 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. machine-

circuit-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.

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,

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.

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


63

automatic or we’re 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.

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

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.


64

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 disease-

respiratory, 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

Don’t assume artefact

Verify hypoxia is real

Systematic approach to diagnosis of hypoxia:

O2 supply

Check pressure gauges, flow meters, FIO2,

vaporizer housing

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


65

High Airway Pressure

A systematic approach to high airway pressure:

Consider the patient context: surgery, pre-

existing 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


66

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 anaesthetist’s ABC

Systematic approach to raised ETCO2

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

Inhaled/exogenous CO2

hypoventilation

increased production


67

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


44

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 doesn’t 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


69

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 doesn’t solve the problem,

the following approach may be useful:

Systematic approach to hypotension:

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

Hypovolaemic

Cardiogenic

Distributive

Obstructive

Trauma

70

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

Trauma

71

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.

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.

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

management can provide important

information, but should not take priority over

management of life threatening injuries. Pre-

hospital 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 patient‟s 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.

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.

Trauma

72

Breathing

If oxygenation / ventilation is inadequate

consider:

Bag / mask ventilation

Decompression of tension pneumothorax

Drainage of haemothorax

Closure of open pneumothorax

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 Hartmann‟s

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)

Disability

Rapid assessment of level of

consciousness using the AVPU score:

A awake

V responding to verbal commands

P responding to painful stimuli

U unresponsive

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.

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.

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 patient‟s 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.

History

The AMPLE mnemonic suggested in the

EMST course provides a useful summary of

the patient‟s history:

A Allergies

M Current Medications

P Past medical history / Pregnancy

L Last meal

E Events / Environment relating to injury

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

Trauma

73

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 re-

evaluation of the patient.

Evolving Injuries

The early response to injury is a dynamic

process. Continual review of the patient‟s

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.

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

Trauma

74

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.

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

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.

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

75

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 12-

36 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.

Trauma

76

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.

Anaesthetic Implications of Chest Trauma

Major chest trauma is usually fatal on scene so

the survivors reaching hospital are a self-

selecting 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.

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

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

77

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 short-

term 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.

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

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

Trauma

78

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

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 costo-

phrenic 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

79

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.

Further Reading

General ATLS: Advanced Trauma Life Support Program

for Doctors. American College of Surgeons

Committee on Trauma. (1994)

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;62:307–310.

Tisherman SA et al .Clinical Practice Guideline:

Endpoints of resuscitation. J Trauma. 2004;57:898-

912.

Ketchum L, Hess JR, Hiipala S. Indications for

early fresh frozen plasma, cryoprecipitate and

platelet transfusion in trauma. J Trauma.

2006;60:S51–S58

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.

http://www.swsahs.nsw.gov.au/livtrauma

http://www.trauma.org/

http://www.emedicine.com/ent/topic488.htm

http://www.swsahs.nsw.gov.au/livtrauma

Trauma

80

Thoracic trauma Meredith JW, Hoth JJ. Thoracic trauma: when and

how to intervene. Surg Clin N Am. 2007;7:95–118.

Neurotrauma Moppett IK. Traumatic brain injury: assessment

resuscitation and early mamgement.Br J Anaesth.

2007;99:18-31.

emac participants manual 2010-1

Documents