British Journal of Anaesthesia 1997; 78: 637–641
CLINICAL INVESTIGATIONS
Inaccurate reporting of simulated critical anaesthetic incidents
A. J. BYRNE AND J. G. JONES
Summary
Eleven anaesthetists completed a simulated anaesthetic which was deliberately complicated by a
slow progressive bradycardia followed by an
episode of severe bronchospasm. After the simulation, each anaesthetist was asked to complete an
anaesthetic chart and a critical incident report.
Considerable discrepancies were found between
the anaesthetists´ written accounts, a videotape of
their performance and actual data from the simulator. During the simulations, all of the anaesthetists
reacted appropriately and treated their “patient”
successfully but their written accounts showed a
tendency to record “typical” rather than actual
events and to ignore events not consistent with
their final diagnosis. Only four anaesthetists mentioned bradycardia in their written description and
none accurately described the changes in arterial
pressure during the episode of bronchospasm. The
findings are in keeping with other studies which
suggest that people record events as “schemata”
rather than as collections of discrete facts. These
results have significant implications for those
involved in the teaching of anaesthesia and in the
analysis of critical incidents. (Br. J. Anaesth. 1997;
78: 637–641).
Key words
Anaesthesia,
audit.
Computers,
simulation.
computer simulation. Anaesthetist, training.
Model,
The Anaesthetic Computer Controlled Emergency
Situation Simulator (ACCESS)1 has been used over
the past 3 yr to provide basic training for junior
anaesthetists and to assess their ability to deal with
critical incidents. The simulator consists of a resuscitation manikin in place of a patient, an anaesthetic
machine/ventilator and computer simulated monitors. The anaesthetic machine is a basic “Boyles
machine” complete with TEC3 vaporizer, which
appears to function normally, but which has been
modified to avoid the use of real volatile agents or
nitrous oxide. A Manley MP3 ventilator was used
during this study. The monitors provide information
on non-invasive arterial pressure, pulse oximetry,
ECG, inspired oxygen concentration and end-tidal
carbon dioxide concentration. Simulations are presented as clinical scenarios which test the ability of
the trainee to deal with a specific emergency. The
simulations are realistic, as judged by those who
have taken part,1 and require appropriate manual
responses to be performed by the trainee, for
example, hand ventilating the lungs of the “patient”
or injecting drugs.
During previous training sessions it was noticed that
trainees often seamed to have misinterpreted the data
presented and, when asked to describe their actions,
their descriptions often contained factual inaccuracies.
However, these inaccuracies were usually plausible
and consistent with their stated final diagnosis. For
example, if they failed to notice a gradual bradycardia,
they often stated that heart rate had been normal
initially and had then changed suddenly.
This study was designed to test if the observed
anomalies arose from the anaesthetist misunderstanding the simulation, from the anaesthetist’s
inability to manage the simulated critical incident, or
if the problem lay in the ability of the anaesthetist to
remember events accurately.
Methods
Eleven trainee anaesthetists, with 3–8 yr clinical
experience, volunteered to take part in a single
simulation, with no opportunity for trial runs or
practice. None had used ACCESS previously and
they were told only that their performance would be
evaluated during a standard simulated anaesthetic.
The same investigator gave each anaesthetist a
verbal introduction to the simulator lasting 3–4 min.
During each simulation, the investigator acted as
a helpful aide, to provide physical assistance for
any task, but not to provide useful diagnostic or
therapeutic information. However, the investigator
did answer questions related to the simulation, for
example, if cyanosis was present or if the breath
sounds had altered in character.
Each anaesthetist was introduced to the simulation as if taking over a routine anaesthetic from a
colleague. They were shown a preoperative assessment form and were told about the anaesthetic
technique being used. The “patient” for each anaesthetist was based on a real case and was young and
healthy. The “operation” was an open reduction and
internal fixation of an ankle fracture, the patient
having had a local anaesthetic ankle block and been
A. J. BYRNE, MRCP, FRCA, Department of Anaesthesia,
Addenbrooke`s Hospital; J. GARETH JONES, MD, FRCP, FRCA,
University of Cambridge and Addenbrooke`s Hospital; Hills
Road, Cambridge CB2 2QQ. Accepted for publication:
December 18, 1996.
Correspondence to A. J. B.
638
paralysed, the trachea intubated and the lungs ventilated 20 min before the anaesthetist taking over the
case. Drugs “used” were thiopentone, vecuronium,
fentanyl and bupivacaine. Each anaesthetist was
allowed to ask questions and to check the settings on
the ventilator, anaesthetic machine and monitors.
The simulation was started as soon as the anaesthetist was familiar with the situation and ended
when the “patient” had been treated correctly and
was stable. Each entire episode was videotaped for
later analysis. At the end of each simulation, each
anaesthetist was asked to immediately complete an
anaesthetic chart and a critical incident report,
covering the period of simulation. They were not
asked questions about any specific event, but were
simply asked to record the simulated events in free
text, as if it were a real case. The computer printed
out a timed list of all significant events and the heart
rate of the “patient” during the period of each simulation. This printed output was not made available to
the anaesthetist.
Each simulation contained two critical incidents:
phase one, a bradycardia and phase two, an episode
of bronchospasm induced by a dose of antibiotic.
During phase one, heart rate started at 80 beat
min1 and decreased in a linear manner, by 10 beat
min1 every 3 min, with only minor random variation. There was no consistent change in arterial pressure. It was expected that at some point the
anaesthetist would administer a dose of anticholinergic drug to correct the bradycardia. When
this dose had been given and bradycardia corrected,
the simulation moved into phase two. The purpose
of the first phase was to compare the actual change
in heart rate (from the simulator printout) with the
change documented on the anaesthetic chart and the
anaesthetist’s perception of events from their written
account.
At the start of the second phase, the anaesthetist
was told that the surgeon had requested that a dose
of i.v. flucloxacillin be given. As soon as the anaesthetist administered some of the flucloxacillin, airways resistance increased markedly, simulating an
episode of bronchospasm. This was manifest by the
Manley ventilator being unable to deliver the set
tidal volume. Arterial pressure remained normal for
two further readings (at least 2 min) and then rapidly
became unrecordable. This simulated a reduced
cardiac output secondary to air trapping and was
based on a real critical incident. It was expected that
the anaesthetists would administer i.v. fluids and
adrenaline, although any reasonable combinations
of treatment would have resulted in the “recovery”
of the “patient”. For example treatment with
salbutamol, aminophylline or adrenaline, in appropriate doses, would all result in a reduction in airways resistance. When these treatments had been
given and the “patient” had stabilized, it was
planned that the simulation would be terminated.
The purpose of this phase was to observe if the
anaesthetists would be aware of the changes in
arterial pressure, if these changes would influence
diagnosis/treatment and if the information would be
recorded in their written account.
The realism of the simulations was assessed by
British Journal of Anaesthesia
asking the anaesthetists to answer two questions,
using a linear analogue score from 1 (unrealistic) to
10 (realistic), in response to the questions “How do
you rate the realism of the simulation?” and “How
do you rate the realism of your responses to the
simulation?”. This assessment was performed to
ensure that ACCESS was providing a level of
realism.
Results
All anaesthetists responded appropriately to the
simulation; all “patients” were treated appropriately
and all simulations were continued to a successful
conclusion.
RESPONSES TO SIMULATED BRADYCARDIA
In the first phase, all 11 anaesthetists diagnosed
bradycardia and administered an adequate dose of
anticholinergic, either atropine 300–600 ␮g or glycopyrronium 200–400 ␮g. However, three anaesthetists failed to document bradycardia and two
failed to record administration of a drug on their
anaesthetic chart.
In the critical incident report, only four of the 11
anaesthetists mentioned bradycardia, and these
comments are reproduced in table 1. Only the first
anaesthetist described the simulation accurately,
with the next two anaesthetists being less specific.
Anaesthetist No. 4 described the actual, gradual
onset of bradycardia as a single rapid episode, with
associated hypotension (which was not present).
Anaesthetist No. 5 ignored the bradycardia and
described an episode of hypotension. (Actual systolic
arterial pressure values shown, at minute intervals,
were: 102, 90, 88, 96, 98, 115, 101, 92, 100, 104
and 110 mm Hg.)
Subsequent inspection of the anaesthetic charts
confirmed that all 11 anaesthetists were unable to
Table 1 Expected and observed descriptions of phase I of the
simulation by anaesthetists (six anaesthetists did not describe
this phase)
Expected
There was a gradual decline in heart rate from 80
to 35 beat min1 over the first 15 min, otherwise
the patient was stable.
Anaesthetist Reported events
(No.)
(1)
(2)
(3)
(4)
(5)
(6-11)
“… gradual decline in HR noted No change in
ECG. No change in BP. No cause evident.”
“One episode of bradycardia during GA,
responded to atropine (300 ␮g) otherwise CVS
O2 Sats 996%.”
“Approximately 40 min into the procedure, which
was otherwise unremarkable other than
bradycardia (sinus) to 42 beat min1. RX
atropine.”
“The first 30 min of anaesthesia and surgery was
stable. The “patient” then developed a bradycardia,
with the heart rate decreasing to about 30 beat
min1. Arterial blood pressure was reduced but still
maintained within acceptable limits.”
“Initially everything was fine, then BP started to
slowly drop from 120 to 90 systolic. Responded to
Hartmann’s 1L.”
No comment made about bradycardia
Inaccurate reporting of simulated critical anaesthetic incidents
639
Table 2 Expected and observed descriptions of phase two of the
simulation by anaesthetists
Expected
After a test dose of flucloxacillin, patient developed
bronchospasm. Arterial pressure was initially
normal but decreased rapidly after 2 min. Patient
responded to i.v. and adrenaline.
Anaesthetist Reported events
(1)
(2)
(3)
(4)
(5)
(6)
(7)
(8)
(9)
Figure 1 Actual and recorded heart rates for anaesthetists Nos
9, 10 and 11.
record accurately the simulated events or their time
scale. Figure 1 shows examples of actual heart rates
plotted on the same scale as those recorded by the
anaesthetist. Overall, subjects tended to record an
initial stable period, followed by a brief bradycardia,
rather than a gradually evolving bradycardia. The
anaesthetists’ charts often showed a time scale twice
as long as the real events.
(10)
(11)
“following i.v. fluclox, Paw increased such that the
Manley was ineffective. A diagnosis of anaphylaxis
was made, Fi O2 to 100%. IPPV by bag.
Auscultation, widespread wheeze bilat. Adrenaline
100 ␮g given i.v. with quick result. As compliance
improved m 9 Manley. 1% ISO throughout. No
desaturation. No hypotension.”
“On administering flucloxacillin 50 mg during
CVS collapse, airway (P) increasedSats
decreased to 91%.”
“I was then asked to administer flucloxacillin
which I did i.v. Over the course of the next few
minutes, the ‘patient’ dropped his SaO2 % to
92–93%, developed bilateral bronchospasm, and
also progressively dropped his blood pressure.”
“‘patient’’ developed bronchospasm hypotension
in response to i.v. flucloxacillin.”
“Asked to give antibiotic. No Hx of allergy.
Diluted flucloxacillin 1 g in 10 ml. 2 ml test dose—
bronchospasm, hypotension.”
“Immediately after flucloxacillin solution 1 ml—
tight bronchospasm with ventilator unable to
deliver volume ... Minimum SaO2 92%, ETCO2 to
3.3 kPa. BP always strongly palpable—minimum
recorded 89/56 (although BP machine
malfunctioned for 2 min during event)”
“Flucloxacillin 1 g i.v. Events: (chronologically)
(1) bronchospasm, (2) no BP recorded, (3) back to
normality”
“After giving test dose of fluclox. ‘patient’ became
difficult to ventilate and was wheezy with very little
air entry suggesting severe bronchospasm.”
“Test dose of 50 ␮g given. ‘Patient’ developed
bronchospam evident by increased Paw and
decreased AE within 30 s. No response to
salbutamol via ETT. Subsequent hypotension (no
BP on Dinamap) but faint carotid pulse.”
“1-ml test dose given 9 bronchospasm 9 hard to
ventilate with halothane, i.v. salbutamol adrenaline fluids.”
“Bronchospasm ‘anaphylactic’ hypotension 2⬚ to
i.v. fluclox ... Min BP 52/min SpO2 92%”
Table 3 Assessment of realism by anaesthetists, using visual
analogue scale (0unrealistic, 10realistic)
Median Range
score
RESPONSES TO SIMULATED BRONCHOSPASM
All 11 anaesthetists described the second phase of
the simulation, but there were significant differences
between actual and recorded events.
In their critical incident reports (table 2), none of
the anaesthetists commented that arterial pressure
had been normal for 2 min after bronchospasm had
started. Only two anaesthetists (Nos 7 and 9) correctly described the actual sequence of events.
Analysis of the videotapes however, showed that
most of the anaesthetists had looked at the arterial
pressure reading soon after bronchospasm had
started. Seven of the 11 anaesthetists either stated
that arterial pressure was normal and/or increased
the inspired concentration of volatile agent, indicating that most were aware of the initially normal
arterial pressure. For example, anaesthetist No. 2
How do you rate the realism of the simulations? 8
How do you rate the realism of your responses
to the simulation?
7
(6–8)
(5–8)
stated “Sats OK, BP OK” just before starting to treat
the bronchospasm with aminophylline. Yet the same
anaesthetist described, in the written account, the
hypotension (“CVS collapse”) as occurring before or
at least at the same time as the bronchospasm.
The answers to the questionnaire (table 3) showed
that the anaesthetists thought that the simulations
were realistic.
Discussion
This study has shown that a group of trainee
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anaesthetists treated a simulated “patient” in a
realistic manner. However, their written accounts of
events were influenced heavily by their own final
diagnosis, with events being altered or omitted to fit
with this diagnosis.
SIMULATED BRADYCARDIA
The results from phase 1 showed a tendency for the
anaesthetists to ignore any events which they perceived as not being directly related to their “main”
problem, in that seven of 11 did not report that
bradycardia had occurred. They also showed a
tendency to “normalize” events. A gradual decrease
in heart rate is unusual, but this was mentioned
by only one anaesthetist who wrote, “No cause
evident”. Anaesthetists Nos 2, 3 and 4 mentioned
that bradycardia had occurred. The implication is
that the anaesthetists were not able to remember
individual values for each of the variables shown, but
were recording events as complete episodes. This
view is reinforced by the recorded values on the
anaesthetic charts (fig. 1) which tended to show an
initial period of normal heart rate followed by
sudden bradycardia. In other words, the first phase
of the simulation had been remembered as two discrete episodes, an initial episode of normality, followed by an episode of bradycardia. When writing
about the events afterwards, values for heart rate and
arterial pressure were obtained from their own
mental models of those events.
This may also explain why anaesthetist No. 5
reported a single reading of systolic arterial pressure
of 88 mm Hg as an episode of hypotension. This was
only a small decrease from the real initial value of 102
mm Hg. However, he reported an initial value of 120
mm Hg, that is a “normal” arterial pressure, which
would make a subsequent systolic pressure of 88 mm
Hg more significant. The next reading of a systolic
arterial pressure of 115 mm Hg may have indicated
that the i.v. fluid had been successful in treating the
“hypotension”, reinforcing the diagnosis. A later
value of 90 mm Hg was then ignored.
SIMULATED BRONCHOSPASM
During phase 2 all anaesthetists responded appropriately to the increased airways resistance and
appeared to be aware of the normal arterial pressure
initially and to make a diagnosis of isolated bronchospasm. Subsequently, when arterial pressure began
to decrease, the anaesthetists seemed to change the
diagnosis from bronchospasm to a generalized
anaphylactic reaction. Then, when their treatment
began to be effective and heart rate and arterial pressure began to return to normal, the new diagnosis of
anaphylaxis with cardiovascular collapse was reinforced. Therefore, the episode was remembered as
an episode of anaphylaxis and any inconsistent information was subconsciously suppressed, or not
remembered.
Within the specialty of anaesthesia, an accurate
record is of prime importance and errors have
tended previously to be described in terms of
inattention or misdiagnosis. This study tested
British Journal of Anaesthesia
anaesthetists during daylight hours, without the distractions of bleeps, telephone calls and audit forms.
The short period of the study also implied that
boredom was unlikely to have been a factor. All
“patients” were treated correctly and the anaesthetists appeared to have few difficulties in understanding the data presented by the simulator.
Although an anaesthetist “taking over” a case half
way through may not be regarded as “best practice”,
trainee anaesthetists are often asked to take over the
care of patients for short periods. This is usually
regarded as acceptable provided the incoming anaesthetist is briefed correctly, as was the case in this
study. The conclusion is therefore that the errors
observed were caused by problems with the recall of
events by the anaesthetists.
The problems described here have been observed
in other fields such as aviation and the nuclear power
industry and have been the subject of considerable
research.2 3 In particular, our limited capacity to
retain numerous discrete elements of data4 and the
tendency of subjects to act on the present value of a
variable rather than the trend5 have been demonstrated. The observation that memories are stored as
typical “patterns” or “schemata” has been described
as far back as 1934.6 The relevance to anaesthetic
practice was described by Allnutt in 1987, “Thus,
with the highest integrity, we soon start reporting not
what happened, but what must have happened”
(authors italics).7
These problems have several important consequences for those analysing critical incidents. First, if
anaesthetists are taught to deal with a list of well
defined emergencies, with their attendant signs,
symptoms and solutions, it is likely that they may try
subconsciously to make any real emergency “fit” one
of this list. Any record of the event may then
resemble the textbook example more than the real
events, with the consequence that vital details may
be obscured. In particular, complications or associations which have not been recognized previously
may continue or go unreported. Second, any aspect
of the real event which was unusual or incompatible
with the diagnosis made tends to be ignored or
reduced in value. Any details recorded tend to
support the final diagnosis.
This study can be criticized for not using real cases
and for the analysed records not haying been made
contemporaneously. However, the anaesthetists
reacted appropriately to the simulations and rated
the experience as realistic. This is reinforced by the
observation that one anaesthetist administered a
dose of neuromuscular blocker to stop a plastic
resuscitation manikin from “coughing”. Although
the records were made immediately after the event
and not at the same time, it is unlikely that during a
real critical incident anaesthetists would have the
time to fill in an anaesthetic chart or to review trends
on a monitor. Therefore, during a critical incident,
when decisions have to be made, anaesthetists have
to rely on their own memory for details of recent
events, and that is what has been tested here.
Finally, our knowledge of anaesthetic emergencies,
their diagnosis and treatment has largely been built
up from analysis of critical incident forms. This study
Inaccurate reporting of simulated critical anaesthetic incidents
indicates that the information derived from that
source may not reflect actual events. Although some
anaesthetic machines are capable of providing
detailed case records, monitors may not provide
accurate readings during a sudden catastrophic event
such as anaphylaxis. In addition, they do not record
all the actions of the anaesthetist. Cases where the
automated record differed substantially from the
events perceived by the anaesthetist may cause difficulties for both trainers and those seeking to defend
against litigation. Automated recording of monitoring and videotaping of the anaesthetic would seem to
provide the best solution, but this is unlikely to
receive widespread acceptance and has significant
cost implications. Overall, the most immediate
solution is for those involved with the analysis of
critical incidents and in the debriefing of the participants to be aware that written and verbal accounts of
events may be inaccurate. In addition, trainers need
to ensure that anaesthetists are aware of the limitations of their perception. In particular, it is vital for
641
anaesthetists to constantly re-check diagnoses and
assumptions as a critical event develops.
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4. Miller GA. The magical number seven plus or minus two:
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