Anaesthesia
for
Medical
Students‐Review
Questions
 
 Chapter
3:
Preoperative
assessment
 
 **Problem
identification
 • Cardiovascular:
ischemic
heart
disease→risk
for
myocardial
ischaemia/infarction
in
 periop
period
 o Hx
for
stability
of
angina

,
exercise
tolerance
 o Consideration
of
valvular
heart
disease,
arrhythmias,
hypertension
 • Respirology:
cigarette,
(stop
for
8
weeks,
but
stopping
for
24
h
still
imparts
benefits)
 o COPD→↑risk
resp
complications;
asthma→bronchospasm;
ensure
no
acute
 URTI
 o Exercise
capacity
by
Hx;
restrictive
lung
dz,
altered
control
of
breathing
 • Neuromuscular:
intracranial
lesion→seek
signs
of
↑ed
ICP
(nausea,
vomiting,
 confusion,
papilledema)
 o Pituitary
lesions,
TIAs/CVAs;
SCI→risk
of
complications
of
failure
and
other
 shit;
lower
motor
neuron
lesions→document
nerve
deficits
before
using
 regional
anaesthesia
 • Endocrine:
DM,
thyroid,
phaeochromocytoma,
adrenal
suppression,

 • GI‐Hepatic:
hepatic
dz,
GERD
 • Renal:
disorders
of
fluid/electrolyte
balance,
renal
failure
 • Haematologic:
anemias,
coagulopathies
 • Elderly:
coexisting
disease
and
diminished
organ
function/organ
reserve
 • Meds/allergies:
need
list!
Generally
pts
can
take
on
day
of
surgery
 o Exceptions;
ASA,
NSAIDs,
insulin,
oral
hypoglycemics,
antidepressants,
MAOi
 • Previous
anaesthetics:
response
to
previous;
FamHx
of
malignant
hyperthermia
and
 plasma
cholinesterase
deficiency
 • Surgery
problems:
pt’s
general
medical
condition
and
anticipated
intraoperative
 problems
 • PhysEx:
focus
on
airway
eval,
CV,
resp,
other
systems
with
symptoms
of
dz
from
Hx
 o General:
physical
and
mental
status
 o Upper
airway:
teeth,
opening
(2
fingers),
thyromental
distance
(3
fingers),
 TMJ
(1
finger)/c‐spine
mobility
(remember
the
3‐2‐1
rule)
 o Lower
airway:
resp
rate,
thoracic
cage,
auscultation,
peripheral
signs
 (clubbing,
cyanosis)
 o CV:
rate,
rhythm,
pressure,
apical
impulse,
JVP,
peripheral
edema,
S1/2,
 murmurs/S3/S4
  Assess
anatomy
for
arterial
line/central
venous/intravenous
access
 • Laboratory
testing:
 o Only
if
indicated
 o CBC
where
signif
blood
loss
anticipated,
suspected
haem
disorder,
recent
 chemo
 o Lytes
if
pt
on
antihypertensive
medications,
or
diuretics,
chemo,
 renal/adrenal/thyroid
disorders


1


o ECG
for
pts>50
or
Hx
of
cardiac
dz,
HTN,
periph
vasc
dz,
DM,
 renal/thyroid/metabolic
dz
 o X‐ray
for
debilitating
COPD,
asthma,
Δ
in
resp
Sx
in
past
6
mos
 o Urinalysis
for
pts
w/
DM,
renal
dz,
recent
urinary
tract
infection


1) Define
the
ASA
physical
status
classification.
 I‐Healthy
pt
 II‐
Mild
systemic
dz;
no
fNal
limitation
 III‐
Severe
systemic
dz;
definite
fNal
limitation
 IV‐
Severe
systemic
dz;
a
constant
threat
to
life
 V‐
Moribund
pt;
not
expected
to
survive
w/
or
w/out
an
operation
for
24
hours
 2) How
long
should
elective
surgery
be
postponed
following
a
myocardial
infarction?
 What
is
the
basis
of
this
recommendation?
 ‐6
months,
according
to
both
Goldman’s
Cardiac
Risk
Index,
and
Detsky’s
Multifactorial
 Index,
and
three
other
cardiac
studies
 
 **Planning
the
anaesthetic
(5
questions
to
ask
about
pt
condition)
 1.
Is
the
pt’s
condition
optimal?
 2.
Are
there
any
probs
which
require
consultation
or
special
tests?
 3.
Is
there
an
alternative
procedure
which
may
be
more
appropriate?
 4.
What
are
the
plans
for
post‐op
management
of
the
pt?
 5.
What
premedication
if
any
is
appropriate?
 3) What
information
should
be
obtained
in
the
anaesthetic
history?
 ‐HPI,
Meds,
Allergies,
PMH/SurgHx,
past
anaesthetic
Hx,
FamHx
of
anaesthetic
probs,
 functional
inquiry,
focusing
on
cardioresp
systems,
NPO
status,
specific
questions
about
 identified
problem
list
 4) What
common
anaesthetic
techniques
can
be
used
to
provide
anaesthesia
for
lower
 abdominal
surgery?
(e.g.
inguinal
hernia
repair)
 ‐general,
spinal
(avoid
intubation→sympathetic
stim
[↑HR/BP],
airway
reflexes
 [bronchospasm])
 5) A)
What
anaesthetic
risks
might
be
associated
in
a
patient
who
smokes
regularly?
B)
 What
information
obtained
from
history,
physical,
or
laboratory
examination
might
 be
useful
in
assessing
this
risk?
C)
Are
there
means
of
decreasing
the
risks
of
 perioperative
complications
related
to
smoking?
 A)
airway
secretions,
asthma,
COPD,
infections
 B)
smoker’s
cough,
wheeze,
medications
for
breathing,
limits
to
physical
activity/exercise
 tolerance,
chronic
infections,
asthma,
COPD,
CXR,
PFT
 C)
“optmize
pt”
 
 Chapter
4:
Premedication
 
 1) Why
are
patients
premedicated
prior
to
surgery?
 ‐pt‐related
reasons:
sedation,
amnesia,
analgesia,
antisialogogue
effect,
↓gastric
 acidity/volume,
facilitate
anaesthesia
induction


2



 1)
ID
any
restricted
mobility
of
the
TMJ‐open
mouth
wide
as
possible
and
note
mobility
at
 mandibular
condyle/TM
joint→space
created
b/t
tragus
of
ear
and
mandibular
condyle
is
 ~1
fingerbreadth
in
width
 2)
Mouth
opening:
at
least
2
fingers.
severe
liver. Insertion
of
the
ETT
through
the
vocal
cords
and
removing
the
laryngoscope
 V.
should
visualize
pharyngeal
arches.
decreased
level
of
consciousness
or

↑ICP.
β‐blockers.
hard
 palate.
 avoid
reflexes
(vagal).
soft
palate. Performing
laryngoscopy
 IV.
bridges.
posterior
pharyngeal
wall
 3)
Thyromental
distance‐thyroid
notch
to
mentum.g.
note
loose/capped/missing
teeth. Confirmation
of
correct
placement.
hemodynamic
 instability/shock.
tonsillar
beds. Opening
patient’s
mouth
 III.
elderly
or
debilitated
pts
 
 Chapter
6:
Intubation
and
anatomy
of
the
airway
 
 1) What
is
the
“1‐2‐3”
test?
 Used
to
assess
several
factors
that
may
affect
decisions
concerning
pt’s
airway
mgmt.‐procedure‐related
reasons:
Abx
prophylaxis.
 obstetrical
pts.
anticholinergic
 ‐coexisting
diseases:
continue
pt’s
own
meds.
nitroglycerine.
 bronchodilators.
with
 tongue
maximally
protruded.
pharyngeal
arches.
corticosteroid
coverage.
tonsilar
beds.
posterior
 pharyngeal
wall
 3) What
structures
are
visualized
in
a
grade
III
laryngeal
view?
 ‐Only
epiglottis
and
a
portion
of
the
arytenoids. Positioning
of
patient
 II.
upper
airway
compromise/resp
failure.
uvula.
and
securing
the
ETT
 
 4) What
is
the
optimal
position
of
the
head
and
neck
for
intubation
using
direct
 laryngoscopy?
 ‐head
and
neck
positioned
using
combination
of
both
cervical
flexion
and
atlanto‐occipital
 extension
(the
“sniffing
position”).
possibly
a
hint
of
the
space
between
the
 vocal
cords
 
 **Tracheal
intubation
 I.
30
general
contraindications
to
use
of
premedication)
 ‐allergy
or
hypersensitivity
to
drug.
gastric
prophylaxis.
thyroid
dz.
Enables
alignment
of
axes
of
mouth/pharynx/larynx
 →permits
direct
visualization
of
larynx
during
laryngoscopy
 5) How
is
tracheal
intubation
confirmed?
 
 3
 .
uvula.
optimize
pt’s
status
prior
to
procedure
(e.
≥
3
cm
preferable
 2) What
does
a
class
I
hypopharyngeal
view
mean?
What
structures
are
visualized
in
a
 class
I
hypopharyngeal
view?
 ‐adequate
exposure
of
the
glottis
during
direct
laryngoscopy
should
be
easily
achieved
 ‐can
see
tongue.
Abx)
 2) What
are
the
general
contraindications
to
the
use
of
benzodiazepine
or
opioid
 premedications?
(p.
renal.
hard/soft
plate.


rather
than
risk
hypoxic
injury
and
gastric
aspiration.
 ensuring
hemodynamic
stability.
analgesia.
PAO2
=
(Patm
–
PH2O)
x
FiO2
–
PaCO2/0.
TAKE
IT
OUT
 If
unsure
of
tube
placement.
and
oxygenation.‐Immediate
absolute
proof→observing
ETT
passing
through
vocal
cords.
than
prematurely
extubating
 pt.
and
increases
up
to
37
 with
increasing
age.
continue
to
support
ventilation.
remove
it
and
resume
mask
ventilation
w/
100%
O2.
observing
CO2
 returning
with
each
respiration.
observing
chest
to
rise/fall
w/
+
pressure
ventilation.
listening
to
apex
of
each
 lung
field
for
breath
sounds
with
ventilation
 
 **IF
IN
DOUBT.
stabilize
 pt
and
call
for
help.
a
VC
of
 15ml/kg
is
needed
to
cough
effectively
and
clear
secretions
 o NIF>
‐25cm
H2O
(normal
negative
inspiratory
force
is
~
‐80
to
‐100
cm
H2O)
 2) What
are
some
important
historical
and
clinical
factors
that
suggest
the
need
to
 intubate
and
ventilate
a
patient?
 
 4
 .
and
there
are
concerns
 about
safe
extubation.
visualizing
tracheal
lumen
through
ETT
using
a
fibreoptic
 scope
 ‐Indirect
confirmation→listening
over
epigastrium
for
absence
of
breath
sounds
with
 ventilation.
LEAVE
IT
IN
 when
considering
extubation
after
pt
was
intubated
for
a
time.
despite
maximum
medical
 mgmt)
 o Respiratory
acidosis
with
pH<7.8
 • Ventilation
 o RR>35/min
in
adults
(muscles
will
fatigue)
 o PaCO2>
60
in
normal
adults
 o PaCO2>
45
in
status
asthmaticus
(and
rising.
5
L.
 
 6) Name
4
simple
manoeuvres
that
can
be
used
to
overcome
an
upper
airway
 obstruction.
 **IF
IN
DOUBT.
 ‐clearing
the
airway
of
any
foreign
material
 ‐using
a
chin
lift
manoeuvre
 ‐using
a
jaw
thrust
manoeuvre
 ‐inserting
an
oral
and/or
nasal
airway
 ‐positioning
the
pt
on
their
side
in
the
semi‐prone
recovery
position
 
 Chapter
7:
Intubation
decisions
 
 1) What
laboratory
criteria
should
you
use
to
assess
the
objective
need
for
intubation
 and
ventilation?
 • Oxygenation
 o PaO2<70
mmHg
with
FiO2
=
70%
 o A‐a
DO2
gradient
>350
mmHg
(normal
is
≤15
mmHg.20
in
COPD
pts
 • Mechanics
 o VC<15mL/kg
(normal
vital
capacity
=70mL/kg
or
approx.
it
is
safer
to
delay
extubation.


 doesn’t
cause
foreign
body
in
trachea
reflex
or
laryngospasm
(when
removed)
 
 Chapter
9:
Rapid
sequence
induction
 
 1) What
is
the
purpose
of
a
RSI?
 ‐used
when
a
pt
req
GA
who
has
been
ID’d
as
having
risk
factors
for
gastric
aspiration:
 ↓LOC.
not
responding
to
 medical
mgmt
in
first
35‐45
minutes)
 
 Chapter
8:
Laryngeal
mask
airway
 
 1) What
is
the
difference
between
a
LMA
and
an
endotracheal
tube?
 ‐LMA:
wide
bore
PVC
tubing
with
distal
inflatable
non‐latex
laryngeal
cuff.
sphincter
incompetence
suspected
(GERD.*
(e.e.
meal
w/in
6
hours.
doesn’t
cause
as
much
trauma
and
positioning
complications
as
ETT.
Prepare
equipment.
drug
overdose
etc..
and
if
pt
in
difficult
position
 to
maintain
mask
anaesthesia
 • Clinical
signs
of
respiratory
failure
and
fatigue
(diaphoresis.
 2.
thermal
burns.
bowel
obstruction.
and
possibly
capnography.
difficult
mask
ventilation.
other
indications
for
ETT
 under
GA
include:
long
procedure.
Consider
pretreatment
agents
based
on
underlying
conditions.
thoracic
cavity
opened.g.
Preoxygenate/denitrogenate:
pt
breathes
100%
O2
for
3‐5
minutes
or
for
4
vital
capacity
 breaths
prior
to
induction
of
anaesthesia
(do
NOT
bag
ventilate)
 5.
 atropine)
 
 5
 .
acute
abdomen)
 2) Describe
the
sequence
of
manoeuvres
used
in
a
RSI.
 4.
can
be
positioned
w/
minimal
anaesthetic
drugs
(doesn’t
req
 muscle
relaxants).
hiatus
hernia.
tachycardia.
 1.g.
in
back
of
pt’s
pharynx
w/
soft
laryngeal
cuff
resting
above
vocal
cords
 at
jN
of
larynx
and
esophagus
 ‐ETT:
gen
req’s
laryngoscope
for
insertion
into
trachea.
and
potential
rescue
devices.• Real
or
impending
airway
obstruction
(epiglottitis.
oximetry.
operative
site
near
pt’s
 airway.
passes
through
vocal
cords
w/
tip
 positioned
in
mid‐trachea
 2) Why
would
a
laryngeal
mask
airway
be
used
rather
than
an
endotracheal
tube?
 ‐pt’s
who
have
no
ID’d
risk
factors
for
aspiration
and
who
do
not
req
intubation
and
 controlled
ventilation
 ‐make
be
difficult
to
obtain
adequate
seal
w/
face
mask
in
pts
w/
no
teeth
or
full
beard.)
 • Tracheal
bronchial
toilet‐pts
who
are
unable
to
clear
their
secretions.
Lidocaine.
mediastinal
 tumours…)
 • Protection
of
airway
(↓LOC.
so
 LMA
good
for
those
pts
 ‐also
LMA
is
easy
to
insert.
cyanosis…)
 • Shock
not
immediately
reversed
with
medical
treatment
(i.
tachypnea.
cardiac
monitor.
inserted
w/o
 special
equipment.
trauma.
pulsus
paradoxus.
COPD
w/
pneumonia)
 • Positive
pressure
ventilation‐during
general
anaesthesia.
 NG
tube).
 accessory
muscle
use.
obesity.
Plan
procedure
incorporating
assessment
of
physiologic
status
and
airway
difficulty.
muscle
relaxants
req’d.
↑ed
abdominal
pressure
(pregnancy.
fentanyl.
Set
up
IV
access.
suction.
the
ETT
 provides
direct
access
for
suctioning
secretions
(e.
 3.


hypoxemia
 2) What
information
can
be
obtained
by
monitoring
the
capnograph?
 ‐Capnometry
is
the
measurement
of
the
CO2
concentration
during
inspiration
and
 expiration
 ‐capnogram
is
the
continuous
display
of
the
[CO2]
waveform
sampled
from
the
pt’s
airway
 during
ventilation
 • Confirmation
of
tracheal
intubation
 • Recognition
of
an
inadvertent
esophageal
intubation
 
 6
 .
head
injury.
diabetes)
 5) What
measures
can
be
taken
to
decrease
the
risk
of
aspiration?
 ‐preop
fasting.
trauma.
pregnant.
(ventilate
when
ETT
 in
place
and
cuff
inflated)
 3) What
is
the
purpose
of
pre‐oxygenation?
 ‐Get
rid
of
nitrogen
and
flood
alveoli
w/
oxygen.
 antiemetics.
hiatus
hernia.
takes
2
minutes
for
a
healthy
pt
to
desat
normally.
or
movement
of
arm
or
leg)
 ‐w/
full
paralysis
w/
muscle
relaxants→
inadequate
anaesthesia
shown
by
HTN.
H2
antagonists/antacids
(↓acidity).
anticholinergics.
Intubate
trachea
after
muscle
relaxation
has
been
achieved.
NG
tube
to
empty
stomach.
CNS
pathology.
↓LOC
 ‐abnormal
anatomy
(Zenker’s
diverticulum.
Provide
postintubation
sedation
and
postintubation
management.
loss
of
blink
reflex
(if
inadequate→facial
 grimacing
to
painful
stimulus.
elderly.
tearing
or
sweating
 ‐excessive
anaesthetic
depth→cardiac
depression
(bradycardia.
Induce
with
potent
sedative
agent.
large
abdo
tumours.g.
consider
cricoid
pressure.
extubation
awake
on
side
 
 Chapter
10:
monitoring
in
anaesthesia
 
 1) What
information
does
the
anaesthetist
use
to
assess
depth
of
anaesthesia?
 ‐GA→lack
of
response
to
verbal
commands.
or
if
 excessive
muscle
relaxant→hypoventilation
and
hypercapnia.
e.
trauma
or
shock)
 ‐impaired
airway
reflexes
(prolonged
tracheal
intubation.
hypotension).
obese.
cricoid
 pressure
on
induction
of
GA.
obesity.
 if
you
can
do
your
shit
right.
preggo.
SCh)
 8.
regional/local
anaesthesia
rather
than
GA.
bowel
obstruction.
metoclopramide
(↓motility).
(Sellick’s
manoeuvre:
 pressure
on
cricoid
cartilage
to
compress
esophaguse
against
C6)
 9.
to
buy
more
time
before
a
pt
desats
<90%.
(45‐60
s
after
muscle
 relaxant
given).
Must
use
cuffed
ETT
to
prevent
aspiration
of
gastric
contents
 10.g.
Give
neuromuscular
blocking
agent
immediately
after
induction.
fear.
ascites)
 ‐delayed
gastric
emptying
(narcotics.
(=fast‐acting
muscle
 relaxant.
 renal
failure.
anaesthesia.
pain.
 myopathies.
 7.
 tachycardia.
 11.
curare)
 ‐↑intragastric
pressure
(preggo.
e.
local
anaesthetic
to
airway.
but
 takes
6
minutes
if
you
preoxygenate
first
 4) Which
patients
should
be
regarded
as
being
at
risk
of
pulmonary
aspiration
of
 gastric
contents?
 ‐↓LOC
(drug
overdose.
Bag‐mask
ventilate
ONLY
if
hypoxic.
CVA.
Confirm
placement
and
secure
tube.6.
labour.
esophageal
stricture)
 ‐↓GE
competence
(NG
tube.


SVR.
myocardial
oxygen
uptake
 ‐∴
good
for
anaesthetic
induction
in
the
severe
asthmatic
pt
or
the
pt
with
cardiovascular
 collapse
requiring
emergency
surgery
 4) What
are
the
concentrations
and
induction
doses
of
thiopental
and
propofol?
 • Thiopental
 o Concentration:
2.
myxedema
 3) When
would
one
choose
ketamine
over
either
thiopental
or
propofol
as
the
 intravenous
induction
drug?
 ‐ketamine
preserves
laryngeal
and
pharyngeal
airway
reflexes
 ‐produces
both
central
sympathetic
stimulation
and
direct
negative
ionotropic
effect
on
the
 heart→↑HR.
coronary
blood
flow.
its
‘redistribution’
from
the
brain
to
other
tissues/organs
 2) Why
would
one
choose
propofol
over
thiopental
as
an
intravenous
induction
agent?
 ‐if
pt
allergic
to
thiopental.
bronchospasm)
 Assessment
of
the
effect
of
cardiopulmonary
resuscitation
efforts
 What
relationship
does
the
ETCO2
value
have
to
the
PaCO2?

 During
GA.
thyroid
storm
 Hypothermia
 Malignant
hyperthermia
 Hypometabolism
 Muscular
activity
 Changes
in
CO2
elimination
 Hyperventilation
 Hypoventilation
 Hypoperfusion
 Rebreathing
 Embolism
 
 Chapter
11:
intravenous
anaesthetic
agents
 
 1) Why
do
pts
awaken
from
a
sleep
dose
of
thiopental
within
5
to
10
minutes
of
its
 administration
when
the
elimination
half‐life
is
of
the
order
of
5‐12
hours?
 ‐b/c
the
thiopental
has
moved
away
from
the
brain
and
is
entering
the
more
slowly
 perfused
organs.
has
status
asthmaticus
or
porphyria.g.
increases
or
decreases
in
ETCO2
values
may
be
the
result
of
either
 increased
CO2
production
or
decreased
CO2
elimination
 
 7
 .5%
(25
mg/mL)
 o Induction
dose:
3‐5
mg/kg
 • Propofol
 o Concentration:
1%
(10mg/mL)
 Recog
of
an
inadvertent
extubation
or
disconnection
 Assessment
of
the
adequacy
of
ventilation
and
an
indirect
estimate
of
PaCO2
 Aids
the
diagnosis
of
a
pulmonary
embolism
(air
or
clot)
 Aids
the
recog
of
a
partial
airway
obstruction
(e.
kinked
ETT)
 Indirect
measurement
of
airway
reactivity
(e.
liver
dz.
the
PaCO2
to
ETCO2
gradient
is
typically
about
5mm
Hg
(PaCO2
5mmHg
 higher).
pulm
art
pressure.• • • • • • 3) • 
 What
conditions
might
result
in
an
ETCO2
measurement
of
20
mmHg
w/
a
PaCO2
 measurement
of
40
mmHg?
(See
right
column)
 ↑ed
ETCO2
 ↓ed
ETCO2
 Changes
in
CO2
production
 Hyperthermia
 Sepsis.g.
BP.

1.
pts
in
renal
failure
 • Giving
SCh→abnormally
high
flux
of
K
(due
to
↑ed
receptors)→acute
rise
in
 potassium
to
levels
as
high
as
13meq/L→sudden
cardiac
arrest
 4) What
is
the
concentration
at
which
SCh
is
supplied?
What
is
the
dose
for
intubation?
 ‐Formulated
at
20mg/mL
 ‐Intubation
dose:
(with
curare
pretreatment)
1.5
mg/kg
IV

 5) Which
drugs
can
be
used
to
antagonize
a
neuromuscular
block?

 
 8
 .
UMN
lesions.5‐3.
M.
severe

closed
 head
injury.
and
is
the
only
drug
of
this
class
that
is
clinically
used
 • Depolarizing
muscle
relaxants
bind
and
depolarize
the
end‐plate
cholinergic
 receptors
 • The
initial
depolarization
can
be
observed
as
irregular.
reduce
to
2.o Induction
dose:
2.
 ‐NON‐depolarizing
neuromuscular
blocking
agents
 • Compete
with
ACh
for
the
cholinergic
nicotinic
receptor
 • As
[]
of
muscle
relaxant
↑
at
the
NMJ.0
mg/kg
  Elderly→≤1
mg/kg
 
 
 Chapter
12:
Muscle
relaxants
 
 1) What
is
the
difference
between
a
depolarizing
and
non‐depolarizing
muscle
 relaxant?
Give
examples
of
each.0
mg/kg
for
healthy.
 
 ‐without
curare
pretreatment→1.
generalized
fasciculations
 occurring
in
the
skeletal
muscles
 2) What
are
the
absolute
contraindications
to
the
use
of
SCh?
 • Inability
to
maintain
an
airway
 • Lack
of
resuscitative
equipment
 • Known
hypersensitivity
or
allergy
 • Positive
history
of
malignant
hyperthermia
 • Myotonia
(M.
neuromuscular
 diseases
like
muscular
dystrophy.
Dystrophyica…)
 • Pts
ID’d
as
being
at
risk
of
a
hyperkalemic
response
to
SCh
 3) Which
pt’s
are
susceptible
to
hyperkalemia
following
SCh?
 • Cholinergic
receptors
located
on
skeletal
muscle
membranes
outside
of
NMJ
can
be
 dramatically
increased
in
number
over
a
24
hr
period
whenever
nerve
impulse
 activity
to
the
muscle
is
interrupted
 • Pts
who
have
sustained
3rd‐degree
burns
or
traumatic
paralysis.5‐2mg/kg
IV
→NOTE:
Initial
dose
of
 succinylcholine
must
be
increased
when
nondepolarizing
agent
pretreatment
used
because
 of
the
antagonism
between
succinylcholine
and
nondepolarizing
neuromuscular‐blocking
 agents.
Congenita.
unpremedicated
pt
  When
premedication
given.
the
intensity
of
muscle
paralysis↑

 • Anticholinesterase
agents
(neostigmine.
severe
intra‐abdominal
infections.5‐2.
edrophonium)
inhibit
the
breakdown
of
 ACh→↑ACh
[]
at
the
NMJ→
competitively
reverse
the
effects
of
a
non‐depolarizing
 neuromuscular
blockade
 ‐Depolarizing
neuromuscular
blocking
agents
 • Succinylcholine
(SCh)
is
most
frequently
mused
muscle
relaxant
used
by
non‐ anaesthetists.


salivation.16%
 Enflurane:
1.
the
minimum
alveolar
concentration
is
the
alveolar
concentration
in
 oxygen
at
one
atmosphere
that
will
prevent
50%
of
the
subjects
from
making
a
purposeful
 movement
in
response
to
a
painful
stimulus
such
as
a
surgical
incision
 ‐it
is
necessary
to
establish
an
anaesthetic
depth
equivalent
to
1.
 diluting
the
O2
present
in
the
alveoli
 ‐when
only
room
air
is
administered
at
the
end
of
the
anaesthetic.
the
body
stores
of
it
are
released
and
flood
the
alveoli.
neostigmine
 o Prevent
breakdown
of
ACh
in
NMJ→competes
with
drug
to
allow
receptor
to
 become
responsive
to
release
of
ACh
from
nerves
 o The
↑ed
[]s
of
ACh
also
stimulate
the
muscarinic
cholinergic
receptors.
pain
with
 splinted
respirations
 
‐∴
administer
100%
O2
at
the
end
of
an
anaesthetic
to
avoid
this
 4) What
are
the
MAC
values
of
isoflurane.
 resulting
in
bradycardia.
and
increased
bowel
peristalsis
 o Anti‐cholinergic
agents
such
as
atropine
and
glycopyrrolate
are
administered
 prior
to
reversal.
this
will
be
faster
with:
 
 ‐rate
of
blood
flow
to
brain
 
 ‐solubility
of
the
inhalational
agent
in
the
brain
 
 ‐difference
in
the
arterial
and
venous
[]s
of
the
inhalational
agent
 3) What
is
diffusion
hypoxia?
 ‐may
result
at
end
of
anaesthetic
 ‐as
nitrous
oxide
is
discontinued.2
to
1.• Muscle
relaxation
produced
by
non‐depolarizing
neuromuscular
agents
may
be
 reversed
by
anticholinesterase
agents
like
edrophonium.
to
block
these
unwanted
muscarinic
effects
 
 Chapter
13:
Inhalational
anaesthetic
agents
 
 1) What
is
MAC?
 ‐Similar
to
ED50.
neuromuscular
blockade.
and
result
in
hypoxemia
 ‐other
causes
of
hypoxemia
include
anaesthetic
agents.75%
 Desflurane:
6%
 Sevoflurane:
2%
 
 
 9
 .68%
 Halothane:
0.
enflurane
and
halothane
in
oxygen?
 Isoflurane:
1.3
of
the
MAC
value
 to
prevent
movement
in
95%
of
pts
 2) What
is
the
relationship
between
the
anaesthetic
concentration
that
is
set
on
the
 anaesthetic
vaporizer
and
the
anaesthetic
concentration
in
the
pt’s
brain?
 ‐the
anaesthetic
tension
cascade
over
time
 ‐the
delivered
[]
tends
to
be
>inspired>alveolar>brain
 ‐increasing
either
the
fresh
gas
flow
rate
or
anaesthetic
concentration
will
result
in
a
faster
 delivery
of
the
inhaled
anaesthetic
agent
to
the
brain
(due
to
a
faster
rise
in
the
alveolar
 concentration)
 ‐amount
of
alveolar
ventilation
(VA=
resp
rate
x
tidal
volume)
 ‐in
terms
of
alveoli→brain
time.
the
dilution
of
O2
may
be
 sufficient
to
create
a
hypoxic
mixture.


What
dose
of
this
drug
would
be
appropriate
to
reverse
 opioid
induced
respiratory
depression?
What.
chest
wall
rigidity.
bradycardia
 ‐slow
GI
motility→constipation/postop
ileus.
bronchospasm.
epinephrine.
deep
breatihing
 ‐vasodilation→↓BP/SVR.
3
with
epi)
 Esters:
chlorprocaine
(11
mg/kg.
used
as
a
preservative
in
local
anaesthetic
solutions.
if
any.
central
neural
 blockade
 4) Why
is
a
vasoconstrictor
often
used
with
a
local
anaesthetic?
Give
an
example
of
a
 LA
vasoconstrictor
and
its
concentration.5
mg/kg.
with
epi→7mg/kg
 
 10
 .
 ↑urinary
bladder
sphincter
tone→postop
urinary
retention
 ‐anaphylaxis.
pruritis
 2) Name
an
opioid
antagonist.
↑biliary
tract
tone→ppt
biliary
colic.
When
would
the
use
of
a
vasoconstrictor
 be
contraindicated?
 • Vasoconstrictor
(e.
ventricular
dysrhythmias
and
cardiac
arrest
 • Continuous
infusion
sof
3‐10
mcg/kg/hr
can
be
used
if
sedation
or
resp
depression
 recur
 
 Chapter
15:
Local
and
regional
anaesthesia
 
 1) Name
2
classes
of
local
anaesthetic
agents.
7
with
epi).
emesis
 ‐resp
depression
(↓rate.
are
any
potential
problems
of
 giving
too
much
of
this
antagonist?
 • Naloxone
(Narcan)
 • Give
small
incremental
doses
of
40
mcg
 • Sudden
reversal
of
the
analgesic
effects
of
opioids
may
result
if
high
doses
of
 naloxone
are
given→abrupt
return
of
pain
can
result
in
HTN.Chapter
14:
Narcotic
agonists
and
antagonists
 
 1) What
undesirable
effects
do
opioids
have?
 ‐may
cause
dysphoric
rxns
when
administered
to
pts
who
are
not
experiencing
pain
 ‐nausea.
intravenous
regional.
and
 may
increase
a
LA’s
potential
neuro‐
and
myo‐toxicities
 3) Name
4
techniques
of
administering
a
local
anaesthetic
drug.
phenylephrine)
used
to
retard
vascular
 absorption
to
reduce
systemic
side
effects
of
LA
 • Epinephrine
[]s
typically
1:100
000
to
1:200
000
 o 1:200
000
has
5mcg/mL
of
epinephrine
 • Vasoconstrictors
contraindicated
in
fingers.
infiltrative.
↑tidal
volume)→slow.
14
with
epi)
 2) What
is
PABA.
and
what
role
does
it
have
in
local
anaesthesia?
 • Para‐aminobenzoic
acid.
and
of
lidocaine
with
a
 vasoconstrictor?
 ‐4mg/kg.
minute
ventilation.
pulm
 edema.
 • Topical.g.
an
give
examples
of
each
 Amides:
lidocaine
(max
dose
4mg/kg.
tachycardia.
bupivicane
(2.
toes
and
penis
 5) Which
regional
block
results
in
the
highest
[]
of
local
anaesthetic
in
the
blood?
 ‐intercostal
nerve
blocks
result
in
the
highest
peak
local
anaesthetic
blood
concentrations
 6) What
is
the
max
recommended
does
of
plain
lidocaine.
peripheral
neural
blockade.


chest/abdo
incision
w/out
pain
mgmt→muscle
splinting.
tachycardia.
↑
smooth
muscle
 tone→gastric
stasis
w/
nausea.
drug
must
pass
through
myelin
sheaths
covering
the
 nerve
roots
 
 ‐dura
acts
as
barrier
to
epidural
LA
moving
into
the
CSF
space
 
 ‐slower
onset
b/c
nerves
are
insulated.
large
net
protein
losses→delayed
wound
healing
 
 
 11
 .
chin
lift/jaw
thrust.7) Why
might
a
regional
anaesthetic
be
given
as
well
as
a
general
anaesthetic?
 ‐for
post‐op
pain
mgmt
 8) Describe
some
of
the
signs
and
symptoms
of
local
anaesthetic
toxicity.
MI
 • ↑symp
tone
also→↑intestinal
secretions.g.
emesis.
consider
 intubation)
 ‐provide
supplemental
O2
(8‐10L/min
for
ambu
bag
ox
flow)
 ‐Assess
the
HR
and
rhythm.
 ‐ensure
clear
airway
(suction.
use
epi
for
profound
 CV
collapse.
apply
monitors
(treat
brady
w/
atropine.
support
BP
w/
ephedrine
or
 phenylephrine)
 ‐stop
seizures
(protect
pt
from
injury
during
seizure.
exterior
to
spinal
fluid).
airways.
mobilization
of
energy
 stores→hyperglycemia.
avoid
hypoventilation→↑LA
uptake.
 • E.
directly
in
contact
with
the
bare
nerve
roots
 
 ‐drugs
produce
a
very
rapid
and
intense
nerve
block
 11)
How
many
milligrams
of
lidocaine
are
in
20
mL
of
a
2%
solution?

 400
mg
 
 Chapter
16:
Acute
pain
management
 
 1) List
the
physiological
effects
of
acute
pain.
consider
diazepam
or
sodium
 thiopental
to
stop
seizure)
 10)
What
is
the
difference
b/t
a
spinal
and
an
epidural
anaesthetic?
 ‐both
are
central
neural
blockade
 ‐epidural
anaesthesia
is
injecting
drugs
into
the
epidural
space
(b/t
ligamentum
flavum
and
 dura
mater.
positioning
in
lat
decub)
 ‐ensure
adequate
ventilation
(bag/mask.
 ‐neurotoxicity→immediate
and
severe
pain→pathologic
damage
to
nerve
 ‐myotoxicity→histological
changes
in
the
tissues.
 ↑contractility/work
 o If
in
setting
of
↓O2
supply→myocardial
ischemia.
but
transient
and
reversible
 9) Describe
the
steps
in
treating
an
acute
local
anaesthetic
toxicity.
administer
bolus
of
ringer’s
lactate.
hypermetabolism.
ileus.
consider
early
electrical
cardioversion
for
arrhythmias)
 ‐Assess
the
BP
and
perfusion‐determine
responsiveness
(if
pt
hypotensive→
 Trendelenburg
position.
slows
gut
motility.
CHF.
produces
less
intense
block
 
 ‐req
5‐10
times
the
amount
of
LA
that
would
be
used
for
spinal
anaesthesia
 ‐spinal
anaesthesia
involves
passing
a
needle
through
epidural
space.
urinary
retention
 • pain→stress
response→hypercoagulable
state→PE.
Ø
 coughing→atelectasis
and
pneumonia
 • Barrage
of
nociceptive
stimuli→↑sympathetic
tone→HTN.
through
dura
and
 into
the
CSF
space‐the
subarachnoid
space.
MI
 o also→↓immunocompetence.


naproxen.
ketorolac
(toradol).
post
traumatic
pain
 syndrome.
disease
states
 • Characterized
by
pain.
[gabapentin.
or
described
in
terms
of
such
damage”
 o So.
relative
contraindication
when
there
is
a
hx
of
 asthma.
ibuprofen.
 acetaminophen)
 5) What
are
the
contraindications
to
administering
a
non‐steroidal
anti‐inflammatory
 drug?
 • Allergy
to
ASA
or
other
NSAID.
respiratory
depression.
nasal
polyps
or
angioedema
 • Renal
insufficiency.
pregnancy/lactation.
 • Ibuprofen
400‐800
mg
PO
q
6‐8
h
 • Ketorolac
10
mg
PO
q
4‐6
h.
max
po
40mg/day
 o 10‐30
mg
IM
q
4‐6
h.
autonomic
disturbances.
delayed
 recovery
of
fN.
↑ed
incidence
of
nausea/vomiting
 4) What
non‐opioid
analgesic
agents
are
available
for
the
control
of
acute
pain?
 • Aspirin.
trophic
changes
 • Common
outcome
of
orthopaedic
injuries
and
industrial
accidents
(but
no
 correlation
b/t
severity
of
injury
and
development
of
RSD.
active
IBD.
indomethacin.
and
tends
to
last
well
 beyond
the
healing
period
of
tissue
injury
 2) What
is
RSD?
What
conditions
may
lead
to
the
development
of
RSD?
 • Reflex
Sympathetic
Dystrophy
 o Variety
of
conditions
including
minor
causalgia.
 Chapter
17:
Chronic
pain
 
 1) What
is
the
difference
b/t
acute
and
chronic
pain?
 • Acute
pain
is
the
nociception
due
to
tissue
injury
and
release
of
nociceptive
agents
 • Chronic
pain
is
an
“unpleasant
sensory
and
emotional
experience
associated
with
 actual
or
potential
tissue
damage.
must
be
promptly
recog’d
 and
treated
 3) What
modalities
are
commonly
used
to
treat
RSD?
 • Early
tx
with
sympathetic
interruption
results
in
pain
relief
and
reverses
the
 pathophysiological
abnormalities
 2) Contrast
intramuscular
and
PCA
opioid
administration
 • Intermittent
IM
administration→wide
fluctuations
in
serum
opioid
concentrations
 →periods
of
over‐sedation
alternating
with
periods
of
poor
pain
control
 • IV
PCA
opioid
administration→
rapidly
adjusted
by
pt→analgesic
[]s
of
opioids
in
 serum
maintained
for
long
periods
of
time
 3) What
are
the
adverse
effects
resulting
from
the
administration
of
excessive
opioid
 analgesics?
 • Sedation.
doesn’t
actually
require
presence
of
tissue
dmg.
peptic
ulcer
dz.
pruritis.
max
IM
120
mg/day
 
 12
 .
bleeding
 disorders
 6) List
an
appropriate
dose
and
schedule
for
two
common
NSAIDs
used
to
control
 acute
pain.
CHF.
Sudeck’s
atrophy.
shoulder
hand
syndrome
 • Ppt
factors
include
accidental/surgical
trauma.
vasomotor
changes.


and
may
be
 exacerbated
by
stretch.
cold.
 Cauda
Equina
Syndrome
 o Disc
herniation.
muscle
spasm.
depressed
reflexes.
deep
and
aching.
saddle
 anaesthesia
 Aortic
aneurysm
 o Leaking.
nausea/vomiting.
Δs
in
mentation
 o ↑
venous
pressure
in
lower
extremities
and
uterus
∴↓uterine
blood
flow
 • aorta
compression→arterial
hypotension
in
uterus→↓uterine
blood
flow→fetal
 distress/asphyxia
 • Prevention:
avoid
supine
position.
psychotherapy.
repair
shit.
tenderness.
 pallor.
loss
of
 bowel
or
bladder
continence.
trigger
points
are
hypersensitive
points
producing
 pain.
tumour
mass.
 immobilize.
judicious
use
of
lumbar
regional
 anaesthetics.
↑
freq
in
3rd
trimester)
 • IVC
compression
causes
↓venous
return
to
heart→signs
of
shock:
hypotension.
and
weakness
 In
affected
areas.
hypersensitivity
to
cold
  Muscle
weakness
or
atrophy
 o Relief
of
Sx
obtained
after
regional
sympathetic
blockade
 What
are
trigger
points?
 In
myofascial
pain
syndrome.
aching
or
throbbing
 o One
or
more
of:
  Vasomotor/sudomotor
changes
  Trophic
changes.
weakness.
which
can
exaggerate
hypotensive
effects
 2) What
factors
may
influence
a
pt’s
experience
of
pain
during
labour
and
delivery?
 o Treat
original
injuries
properly
and
rapidly
(remove
foreign
bodies.
stiffness.
lies
on
side.
edema.
viral
illnesses
or
direct
pressure
 Name
2
surgical
conditions
that
may
present
w/
back
pain
and
require
emergency
 surgical
intervention.
sweating.
dissecting.4) • 5) • • 6) • • 
 Chapter
18:
Obstetrical
anaesthesia
 
 1) What
is
supine
hypotensive
syndrome?
How
can
it
be
prevented?
 • When
the
gravid
uterus
compresses
the
IVC
and/or
aorta
when
the
parturient
lies
in
 the
supine
position
(about
15%
of
pts
as
early
as
20t
week.
relieve
pain)
 o Tx
modalities
include
early
use
of
sympathetic
blocks.
abscess
 o Signs:
neuro
deficit
in
lower
extremities
(paralysis.
stress.
loss
of
sensation).
taut
muscle
bands
may
be
palpable.
ruptured
 
 13
 .
surgical
sympathectomy
 
 How
is
a
dx
of
RSD
made?
 Criteria
are
 o Hx
of
recent
or
remote
accidental
or
iatrogenic
trauma
or
dz
 o Pt
complains
of
persistent
pain
that
is
burning.
physio.
are
called
TPs
 o Pain
from
these
is
described
as
steady.
fatigue.
 medical
therapy
and
if
these
fail.


sedatives.
and
risk
of
hypoxemia
and/or
pulmonary
 aspiration
of
gastric
acid
 • GA
creates
potential
of
having
maternal
drugs
transferred
to
neonate→neonatal
 depression
and
need
for
resuscitation
 
 Chapter
19:
Basic
neonatal
resuscitation
 
 1) What
is
the
Apgar
score
of
a
baby
that
is
limp.
size
and
anatomy
of
 pelvis.
mental
preparation.
use
of
medications
to
augment
labour
(e.
primi
vs
multipara.
education
(expectations.
medical
support.
the
gentle
stimulation
will
also
help
 initiate
and
maintain
breathing
 • Physical
stimulation
 o If
drying/suctioning
do
not
induce
effective
breathing→gentle
 slapping/flicking
of
soles
of
feet.
if
<100bpm.
partner.
or
rubbing
infant’s
back
may
be
useful
 o Do
not
waste
time
continuing
tactile
stim
if
no
response
after
10‐15
s
 • Evaluate
the
infant
 o Respirations:
apneic
or
gasping
infants
(despite
brief
stim)
should
receive
 positive
pressure
ventilation
(PPV)
 o Heart
rate:
monitor
by
auscultation
or
palpation.
monitor
heart
rate
for
bradycardia.
behavioural
 modification
(psychoprophylaxis‐Lamaze).
Activity
 (Muscle
tone).
dry
the
infant.
all
parturients
considered
to
have
 potentially
difficult
airway
to
intubate
 • GA
introduces
risks
of
failed
intubation.
 • Keep
the
infant
warm
and
dry
 o Overhead
radiant
heater.
HR<100‐1.
 • Open
the
airway
 o Positioning.
 classes).
blue.• Psychological
state.
oxytocin).
opioid
analgesics
(+/‐
antiemetics).
 consider
special
endotracheal
suctioning
in
depressed
infant.
Grimace
(reflex
irritability).
duration
of
labour
 3) What
options
are
available
for
dealing
with
the
pain
of
labour
and
delivery?
 • Nothing.
psychological
support
(coaches.
 even
if
infant
making
some
respiratory
efforts
 o Colour:
presence
of
central
cyanosis
means
infant
not
well
oxygenated.
a
heart
rate
of
60
bpm.
Colour‐0.g.
has
no
response
to
 oropharyngeal
suctioning.
Pulse
(HR).
Reflex
irritability‐0.
 provide
face
mask
w/
O2
at
5
L/min
until
infant
becomes
pink
 
 14
 .
hypnotherapy.
walking.
family
support.
family
members).
suction
mouth
then
nose.
cultural
 background.
spinal
anaesthesia.
massage.
general
anaesthesia
 4) What
are
the
major
risks
of
general
anaesthesia
in
the
parturient
undergoing
a
 caesarean
section?
 • All
parturients
considered
to
have
full
stomach
and
gastric
precautions
including
RSI
 are
indicated
with
GA
 • Upper
airway
edema
occurs
in
pregnancy.
Respiration‐1
=
2
 2) Describe
the
basic
steps
in
neonatal
resuscitation.
and
irregular
gasping
respiratory
 efforts?
 • APGAR:
Appearance
(colour).
size
and
presentation
of
fetus.
Respiration

 • Muscle
tone‐0.
begin
PPV.
epidural
 analgesia.


what
is
the
[]
and
dose
of
epinephrine.
other
hand
supports
back
 below
 o Pressure
enough
to
achieve
1. Intravenous
fluids
 3.
 • Ventilatory
support
required
when
apnea
or
gasping
respirations
are
present.25
mL
to
0.1mg/mL
dilution
 • IV
dose
is
0.1‐ 0.
 **Adequate
ventilation
is
assessed
by:
 ‐Observing
chest
wall
motion
and
hearing
breath
sounds
bilaterally
 
 **When
should
I
start
chest
compressions?
 ‐when
HR
remains
<80bpm
despite
PPV
with
100%
O2
 ‐chest
compressions
can
be
discontinued
when
the
HR
is
≥80
bpm
 
 **What
is
the
proper
technique
for
administering
chest
compressions
to
an
infant?
 • 2
methods
 o thumb
method:
fingers
around
back.01
to
0. Epinephrine
 4.5
cm
of
displacement
 o 120
compressions
per
minute
(2/sec)
 
 **The
4
common
drugs
used
in
resuscitation
of
the
depressed
neonate:
 1.
epi
can
be
given
through
ETT
 o Should
be
diluted
w/
1‐2
mL
of
saline
 o If
infant
does
not
respond
to
initial
ETT
dose.03
mg/kg
 • In
a
3
kg
infant. Oxygen
 2.
with
 downward
displacement
of
sternum
 o Two
finger
approach:
middle
and
ring
fingers
of
one
hand
perpendicular
to
 chest
as
finger
tips
apply
pressure
to
sternum.
0.
thumbs
side
by
side
over
sternum.75
mL
of
epinephrine
would
be
an
appropriate
starting
 dose
 • If
IV
route
unavailable.2
mg/kg)
 
 
 
 15
 3) When
is
positive
pressure
ventilation
(PPV)
indicated
in
the
newborn
infant?
 Describe
the
technique
of
PPV.
increase
by
a
factor
of
10
(0.
or
central
cyanosis
persists
despite
100%
O2
 • Most
neonates
can
be
adequately
ventilated
w/
a
bag‐mask
 o The
assisted
ventilatory
rate
should
be
b/t
40‐60
breaths
per
minute
 o Initial
lung
inflation
pressures
may
be
as
high
as
30‐40
cm
H2O
to
overcome
 the
elastic
forces
of
the
lungs
if
the
infant
has
not
take
its
first
breath
 o Subsequent
ventilation
should
be
achieved
with
airway
pressures
of
15‐20
 cm
H2O
 . Naloxone
 
 4) Assuming
a
newborn
infant
weighs
3
kg.
the
 HR
is
<100bpm.
and
 how
ought
it
be
administered?
 • Epinephrine
[]
in
neonate
resuscitation
is
supplied
as
0.

g.
 • Crystalloid
solutions
are
salt
containing
solutions
that
are
semipermeable
to
cellular
 membranes
 o E.
femur.
 • Fractured
hip.
and
the
accepted
minimal
hemoglobin
after
surgery
is
 80g/dL.
pelvis.g.
pts
with
Hb
<110
g/L
and
pts
 with
unstable
angina
or
critical
aortic
stenosis
 5) Calculate
the
acceptable
amount
of
blood
that
can
be
lost
in
70
kg
male
if
his
initial
 hemoglobin
is
140
g/dL.
whole
blood
 4) Which
pts
should
consider
autologous
blood
donation?
For
which
patients
is
this
not
 suitable?
 • Preop
collection
of
blood
from
a
pt
who
is
scheduled
to
have
surgery.
albumen.
plasma.
(citrate
toxicity.
pancreatitis
 3) What
is
the
difference
b/t
a
crystalloid
and
a
colloid?
Give
examples
of
each.
bowel
obstruction.
“2/3.
e.
NS.
 • Whole
blood:
autologous
 • Fresh
frozen
plasma:
indicated
to
replace
certain
factor
deficiencies
 • Platelets:
after
massive
transfusion.
trauma.
dextran
 o May
be
collected
from
donor
blood
pool.
and
for
whom
 one
anticipates
the
need
for
a
perioperative
blood
transfusion
 • Not
suitable
for
pts
w/
bacterial
or
viral
infections.
e.
preoperative
bowel
prep.
hetaspan
(?sp).
pentaspan.
 • WBCs
(febrile
reaction)
 hyperkalemia.
 protracted
vomiting
and
diarrhea.
RL.
dilutional
 • Volume
(circulatory
overload)
 coagulopathy)
 • Cold
(hypothermia)
 • Platelets
(dilutional
coagulopathy)
 • RBCs
(major/minor
reactions)
 • Biochem.
sepsis.
associated
with
abnormal
bleeding
and
 dilutional
thrombocytopenia
 
 **Potential
complications
of
blood
transfusions
 • Air
(embolism)
 • Plasma
(Allergic
rxn.
burns.
 • ABL
=
(Hbi‐Hbf)/Hbi
x
EBV
 o =(140‐80)/140
x
(70ml/kg
x
70kg=4900ml)
=
2100
mL
 6) What
is
the
most
common
cause
of
an
ABO
incompatible
blood
transfusion?
 ‐clerical
error
in
patient
and
blood
identification

 7) Name
3
different
blood
components
that
may
be
transfused.
hypoCa)
 
 16
 .Chapter
20:
Intravenous
fluid
and
blood
component
therapy
 
 1) How
are
the
hourly
and
daily
maintenance
fluid
requirements
calculated?
 Maintenance
water
requirements
 
 Per
hour
 Per
day
 1st
to
10th
kg
 4ml/kg
 100ml/kg
 11th
to
20th
kg
 2ml/kg
 50ml/kg
 21st
to
nth
kg
 1ml/kg
 20ml/kg
 
 2) List
conditions
that
may
be
associated
with
a
significant
preoperative
fluid
deficit.
1/3”
IV
solutions
 • Colloid
IV
solutions
contain
aggregates
of
molecules
that
resist
diffusion
across
 cellular
membranes
 o May
be
synthetic.g.


 Shock
(Tintinalli’s)
 Type
 
 Comment
 Hypovolemic

Caused
by
inadequate
circulating
volume
 Cardiogenic

 Caused
by
inadequate
cardiac
pump
function
 Obstructive
 Caused
by
extracardiac
obstruction
to
blood
flow
 Distributive
 Metabolic
derangements
that
impair
cellular
respiration
such
as
cyanide
 toxicity.• Microaggreg.
 and
an
increase
in
cardiac
output
 o Most
common
form
of
this
type
is
septic
shock.
residual
paralysis.
 parasitic)
 • Immune
(immune
suppression)
 
 Chapter
21:
Common
perioperative
problems
 
 **
Severe
bradycardia
must
be
assumed
to
be
secondary
to
hypoxemia
until
proven
 otherwise
 
 1) Define
shock.
sepsis.
Classify
the
different
types
of
shock
and
give
examples
of
each.
as
a
result
of
a
 myocardial.
viral.
valvular
or
electrical
problem

 o Myocardial
infarction
is
the
most
common
cause.
depending
on
the
cause
 
 Chapter
22:
Managing
the
circulation
 
 1) What
are
the
broad
goals
in
controlling
the
circulation?
 • The
principle
goal
of
circulatory
support
is
to
optimize
tissue
perfusion
with
 oxygenated
blood
 
 17
 .
with
low
central
venous
 pressure
and
low
pulmonary
capillary
wedge
pressure
 • Distributive
shock
is
characterized
by
systemic
vasodilation.
and
hypoxemia
are
all
 potent
stimulants
which
can
produce
an
agitated
state
 • Common
causes
of
agitation
in
elderly
pts
are
pain
and
bladder
or
bowel
distension
 • Excessive
sedation
can
be
treated
with
reversing
agents.
(Dyspnea)
 • Infections
(bacterial.
PCWP
and
SVR
 • Obstructive
shock
occurs
when
there
is
an
obstruction
preventing
cardiac
filling
or
 emptying
 o Two
immediately
treatable
causes
of
it
include
a
tension
pneumothorax
and
 cardiac
tamponade
 
 **Nausea
and
vomiting
perioperatively
must
be
assumed
to
be
secondary
to
bradycardia
 and
hypotension
until
proven
otherwise
 
 2) What
are
some
treatable
causes
of
an
agitated
postop
state?
 • Upper
airway
obstruction.
where
ateriovenous
shunting
 at
the
tissue
level
results
in
an
accumulation
of
lactic
acid
and
tissue
anoxia
 • Cardiogenic
shock
when
heart
fails
to
perform
its
pumping
function.
hypercarbia.
where
characteristic
 findings
include
an
increase
in
CVP.
 • Hypovolemic
shock‐
the
most
common
type
of
shock.
relative
hypovolemia.


e.
gut.
the
heart
rate.
bronchitis
 • Increased
shunt
 o Perfusion
of
alveoli
without
ventilation.
myocardial
conduction
and
contractility
 What
are
the
factors
which
determine
cardiac
output?
 CO
=
HR
x
SV
 The
determinants
of
cardiac
output
are
preload
(the
end‐diastolic
stretch
of
the
left
 ventricle).
one
must
assess
and
optimize
the
preload.
afterload.
 Alpha‐1.
ensuring
a
consistent
 inspired
oxygen
concentration
 o Should
use
a
double
flow
setup
or
a
non‐rebreathing
face
mask
w/
reservoir
 bag
when
>50%
inspired
O2
[]
is
required
 • The
ambu
bag
and
mask
unit
is
used
for
providing
primary
airway
mgmt
in
pts
 requiring
positive
pressure
ventilation
and
oxygenation
 o Can
be
used
as
the
primary
system
for
airway
mgmt
in
the
pt
requiring
 ventilatory
support
 3) List
the
five
categories
of
conditions
causing
hypoxemia.
heart
 rate.
isoproterenol
 o Increased
heart
rate.
non‐rebreathing
face
 mask
with
reservoir
bag
 2) When
should
a
puritan
face
mask
be
used?
When
should
one
use
a
manual
 resuscitation
device.
contractility.
Oxygen
therapy
and
hypoxia
 
 1) List
some
devices
that
are
commonly
used
to
deliver
oxygen
to
spontaneously
 breathing
patients.
simple
face
mask
oxygen.
CHF.g.
liver
and
heart
 Beta‐1.
e.
oxygen
transport
and
organ
perfusion
 What
are
the
differences
b/t
an
alpha‐1
and
beta‐1
adrenergic
agonist?
Give
 examples
of
each.
emphysema.
phenylephrine
 o Vasoconstriction
of
the
skin.g.
and
the
 afterload
(the
myocardial
wall
stress
of
the
left
ventricle
during
ejection)
 
 Chapter
23.
kidney.
e.
atelectasis.2) • • 3) • • o To
achieve
this.
 Hypoxemia:
low
level
of
O2
in
the
blood
 • Decreased
FiO2
 o ↓ed
inspired
O2
concentration
or
↓ed
barometric
pressure
(altitude)
 • Decreased
alveolar
ventilation
 o Hypoventilation
(2°
to
sedative
drugs
or
pain
is
common)
 • Increased
dead
space
ventilation
(ventilation‐perfusion
inequality)
 o Responds
to
supplemental
O2
therapy
 o Causes
include
hypovolemia
and
high
airway
pressures
with
PPV
 o Pulmonary
embolism.
such
as
an
ambu
bag
and
mask
unit?
 • The
puritan
mask
delivers
the
highest
level
of
humidified
oxygen
 o Oxygen
flow
rates
of
>30L/min
can
be
achieved.
the
contractility
(the
myocardium’s
intrinsic
ability
to
 perform
work
at
any
given
level
of
end‐diastolic
fibre
length
[preload]).g.
 pneumonia
and
endobronchial
intubation
with
lobar
collapse
 
 18
 .
 • Nasal
prongs.
Venturi
face
mask.
aspiration.


emphysema.
carbon
dioxide
production
and
heat
 result
in
desaturation
or
cyanosis.
interstitial
pulmonary
pathology
(e.
obstructive)
 • Cellular
hypoxia

 o Histotoxic
poisoning
(e.
elevated
end‐tidal
CO2
values
and
rapid
 increases
in
temperature
 2) List
2
anaesthetic
agents
that
may
trigger
an
MH
reaction.
blood.
or
tissues
 • Decreased
functional
hemoglobin
 o Anemia.
anemia.
cardiogenic.g.
halothane.
cyanide)
 
 Chapter
24:
Unusual
anaesthetic
complications
 
 1) What
is
MH?
 • A
rare
clinical
syndrome
that
has
been
observed
during
GA
 o Acute
fulminant
form.
severe
exercise
 o Pulmonary
fibrosis.
 sarcoidosis)
 4) List
the
four
categories
of
conditions
causing
hypoxia.
sevoflurane)
 3) Which
drug
is
used
specifically
to
treat
an
MH
reaction?
 • Dantrolene‐skeletal
muscle
relaxant
(every
hospital
that
provides
GA
services
is
 req’d
to
keep
a
current
stock
[minimum
36
vials]
of
dantrolene
available
in
their
 pharmacy
department)
 4) What
strategies
are
useful
in
reducing
the
perioperative
risk
of
pulmonary
 aspiration
of
gastric
contents?
 • Avoid
impairing
airway
reflexes
(choose
local
or
regional
anaesthetic)
 • Reduce
gastric
volume
and
acidity
 o Fasting.
distributive.
hemoglobinopathies
 • Decreased
PaO2
 o Hypoxemia
 • Decreased
tissue
perfusion
 o Shock
states
(hypovolemic.
antacids
(sodium
citrate).
topicalization
and
local
anaesthetic
 blocks
of
the
upper
airway
reduces
chance
of
failed
intubation.
 • The
ABCs
for
anaphylaxis:
 
 19
 .
 • SCh
(depolarizing
muscle
relaxant)
and
any
of
the
volatile
anaesthetic
agents
 (isoflurane.
enflurane.
difficult
mask
 ventilation
and
subsequent
gastric
aspiration
 • Pts
w/
ID’d
risk
factors
for
gastric
aspiration
who
require
GA
must
have
RSI
(see
 above)
 5) Describe
the
steps
used
to
treat
an
anaphylactic
reaction.g.
H2
blockers.• Decreased
diffusion
 o High
altitude.
triggered
by
certain
anaesthetic
 drugs→hypermetabolic
state
due
to
acute
uncontrolled
skeletal
muscle
 metabolism
 o Rapid
increases
in
O2
consumption.
 Hypoxia:
low
level
of
O2
in
the
air.
 gastric
emptying
by
NG
tube
 • In
pts
with
anticipated
difficult
intubation.
gastric
motility
agents.

0
mg
IV
with
CV
collapse
 o Epi
infusion
0.05‐0.
or
methylprednisolone
1
mg/kg
IV
q6h
x
24
h
 o Inhaled
salbutamol
for
bronchospasm
 o Avoid
beta
blockers
 
 20
 .
may
req
2‐4
L
for
a
70
kg
adult.

 o Airway.2
mcg/kg/min
 o Crystalloids
(NS.
i.5‐1.
and
adrenaline
 o Breathing.
25‐50ml/kg
 o Diphenhydramine
50
mg
iv
 o Cimetidine
300
mg
IV.
and
Benadryl
 o Cyrstalloids
and
cimetidine
 o Steroids
 • Mgmt
of
anaphylaxis
during
anaesthesia
 o Stop
drug
or
allergen
administration
 o Provide
100%
O2
 o Discontinue
surgery
and
anaesthesia
as
soon
as
feasible
 o Give
epi
50‐100
mcg
IV
with
hypotension.
0.
RL)
IV.
or
ranitidine
50
mg
IV
 o Hydrocortisone
100
mg
IV.e.

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