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Special Techniques and
Concepts in Anesthesia
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3
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ANESTHESIA
AND THE PREGNANT PATIENT
Postpone all elective surgery until 6 weeks following delivery. The risks of
teratogenesis and/or preterm labor are too high to consider elective surgery
prior to delivery.
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Depending on
the severity
or emergent
nature LLC
of an operative procedure,© Jones & Bartlett Learning, LLC
NOT
FOR SALE
OR
DISTRIBUTION
fetal and uterine
monitoring
may be
warranted
(e.g., in women who are moreNOT FOR SALE OR DISTRIBUTION
than 16 weeks pregnant) throughout the surgery, with plans and preparation for
an emergency cesarean section (C-section) if necessary.
Later in pregnancy, the goal is to prevent fetal asphyxia by maintaining a
©maximum
Jones &delivery
Bartlett
LLC
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& the
Bartlett Learning, LLC
of Learning,
oxygen to the
mother and, therefore, the
fetus via
NOT
FORMaintain
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DISTRIBUTION
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placenta.
maternal
blood pressure to ensure adequate
placental
perfusion. In evaluating laboratory values, the total blood volume will be
increased; therefore, one would expect a reduction in hemoglobin and hematocrit values. Blood gases normally show a respiratory acidosis.
Use Learning,
left uterine displacement
(LUD) to prevent
compression
on the
aorta
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when
theDISTRIBUTION
mother is in the supine position (in women
who are
moreOR
thanDISTRIBUTION
16–20
NOT FOR SALE
OR
NOT FOR
SALE
weeks pregnant).
Tocolytics are drugs that suppress onset of premature labor and should be
available when giving anesthesia on any pregnant patient. They include the following medications:
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•
•
•
•
FOR
SALE
ORcalcium
DISTRIBUTION
Magnesium NOT
sulfate:
first-line
agent;
antagonist.
Ritodrine: beta-2 agonist; decreases levels of free calcium
Terbutaline: beta-2 agonist
Calcium-channel blockers: nifedipine, verapamil
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Anesthetics
in Pregnancy
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General anesthesia helps to block uterine contractions. Use lower doses of all
medications. Short-acting agents are preferred and minimize overall exposure
to all anesthetic agents.
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Page 18
Chapter
3 Special
Techniques and Concepts
in Anesthesia
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& Bartlett Learning, LLC
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Learning,
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NOT
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Narcotics cross the placental barrier and affect
the fetus.
Hypotension occurs in the distal aortic segment
(below the clamp), with MAP decreasing by 15%.
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Spinal blood flow decreases:
Muscle relaxants
do notSALE
cross OR
the DISTRIBUTION
placental
NOTplacement
FOR SALE
OR DISTRIBUTION
NOT FOR
Proximal and distal clamp
to isolate
barrier as readily as narcotics.
the diseased aortic segment may include critical
intercostal vessels that provide flow to the cord;
Avoid benzodiazepines (owing to the increased
this loss is not compensated for by distal perfuincidence of deformities in the fetus) and nitrous
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LLC
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& Bartlett
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sion. The
following
measures Learning,
are directed
at
oxide in&
any
pregnantLearning,
patient.
NOT FOR SALE OR DISTRIBUTION
NOT
OR DISTRIBUTION
protecting
the FOR
spinalSALE
cord when
the cross-clamp
Regional anesthesia is preferred because it miniis on:
mizes fetal exposure to the anesthetic agents and
• Maintain MAP at 40–60 mm Hg.
reduces the risk of maternal aspiration.
• Use somatosensory evoked potentials (SSEPs)
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© Jonesto
&monitor
Bartlett
Learning, LLC
dorsal column function (sensory
AORTIC
CROSS-CLAMPING,
SPINAL
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tracts).
Anterior
cord function (i.e., motor tracts)
CORD ISSUES, AND AORTIC SHUNTING
is not monitored with SSEP.
Application and Withdrawal of an Aortic
• Motor evoked potentials (MEPs) can accurately
Cross-Clamp
monitor anterior horn function. However,
The higher the ©
cross-clamp
the aorta
(at the LLC muscle relaxants cannot
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given when
suprarenal or supra-celiac
more
severe
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NOT FORlevels),
SALEtheOR
DISTRIBUTION
monitoring MEPs.
the effects. Fewer hemodynamic changes occur
• Hypothermia (decreasing core temperature to
when cross-clamping the infra-renal aorta.
33–34°C) will lower the patient’s metabolic
rate. It can be accomplished with application
Prior to Clamp Placement
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Jones
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of ice©
and
administration
of cold
blood. Care
The systolic blood pressure (SBP) should be
NOT
FOR SALE OR DISTRIBUTION
FOR
OR DISTRIBUTION
must NOT
be taken,
as SALE
the myocardium
becomes
90 mm Hg prior to clamp placement. Minimize the
irritable at 32°C.
effects of clamping with nitroprusside, nitroglycerin,
•
Spinal drains can be used to relieve
betablockers, fenoldopam, nicardipine, and/or
pressure. The pressure exerted by the
inhalational agents.
fluid (CSF) increases
during
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AfterOR
Clamp
Is Applied
cross-clamping.
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Marked hypertension occurs in the proximal aortic
• Give steroids to further protect the
segment (above the clamp).
spinal cord.
•
•
•
•
•
MAP increases by 40%.
Renal and intestinal blood flow decreases:
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Learning,
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Acute elevations
in left ventricular
pressure
occur. LLC
To prevent renal failure and gut ischemia, keep the
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FOR
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OR
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Cardiac output is decreased.
patient’s BP up with good perfusion. Give Mannitol
CVP increases by approximately 4 mm Hg.
(0.5 mg/kg), furosemide, and IV infusion of lowLeft atrial pressure (LAP) and pulmonary
dose dopamine or fenoldopam for renal protection.
capillary wedge pressure (PCWP) increase
Even if aortic shunting is used, the distribution
12 mm Hg
or more. Learning, LLC
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& Bartlett
& Bartlett
Learning,
LLC
changes ©
in Jones
renal blood
flow make
these interven• Coronary
blood flow
by 40%.
NOT
FOR SALE
OR increases
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FOR
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OR
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tions prudent.
• Systemic vascular resistance (SVR) increases
by 100%.
Before Clamp Is Removed
• Levels of catecholamines, renin, and angiotensin
Check the volume load. The patient may need vasoincrease,
leading
to
vasoconstriction.
pressors
prior toLearning,
removal of the
cross-clamp.
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Page 19
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Spinal Cord
Injury and
Aortic Cross-Clamping
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19
Aortic Cross-Clamp Removal Effects
The artery of Adamkiewicz joins the anterior spinal
artery in sending flow to the lower thoracic and
Declamping shock is a possibility. Severe
© Jones & Bartlett Learning,lumbar
LLC segments T8–L4: the© celiac
Jones
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artery
at T12 Learning, LLC
hypotension—a decline in BP of as much as 70%—
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(gastric, splenic, hepatic branches), the superior
may occur due to hypovolemia (combined with
mesenteric artery at L1, and the inferior mesenbleeding), with this abrupt decrease in after load.
teric artery at L3. The lateral aortic branches are
The release of vasodilating acid metabolites from
the suprarenal and renal branches at L1 and the
the ischemic lower body into the general circula© Jones & Bartlett Learning, LLC
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gonadal branchat
L2. &
The
posterolateral
artery
tion (noted as an increase in ETCO2 ), the release of
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contains
the
inferior
phrenic
and
lumbar
branches.
vasodilator substances, and an increase in the vasMaintaining perfusion in these areas can be imporcular space all cause a severe decrease in ventricutant, particularly in thoracoabdominal aneurysm
lar preload. Declamping shock is also associated
repair, where the cross-clamp is applied above
with hyperkalemia and hypocalcemia.
these structures.
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Learning,
LLC
©
Jones
& Bartlett Learning, LLC
Removal of the cross-clamp may also lead to
feared
complication of aortic
NOT FOR decreased
SALE ORcontractility
DISTRIBUTION
FORmost
SALE
ORmajor
DISTRIBUTION
and cardiac output. The NOT The
cross-clamping
is
paraplegia
from prolonged spinal
severity of this effect is influenced by the duration
cord ischemia as a consequence of hypotension
of clamping, existence of adequate preload, and
and surgical interruption of the blood supply to
influence of circulating drugs.
artery of Adamkiewicz. Along
with &
paraplegia,
©removal
Joneseffects
& Bartlett
Learning,the
LLC
© Jones
Bartlett Learning, LLC
Treat cross-clamp
by decreasing
there
is
a
risk
of
mesenteric/bowel
ischemia/
NOT FOR SALE OR DISTRIBUTION
NOT
FOR SALE
OR DISTRIBUTION
the anesthetic levels,
decreasing
or discontinuing
infarction,
renal
ischemia/failure,
and hepatic
vasodilators, and administering volume (crystalischemia.
Coagulopathy
can
occur
if
thoracolumbar
loids, colloids, cell saver, blood products), and
blood flow is decreased when systemic pressures
calcium chloride. May also need to give phenyleare low. Maintaining
perfusion
pressure
phrine,
epinephrine,
or norepinephrine
maintain
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& Bartlett
Learning, to
LLC
© Jonesa&distal
Bartlett
Learning,
LLC
mean
of
70
mm
Hg
or
higher
will
minimize
the
incitheNOT
BP. Increasing
the OR
ventilation
rate will help
FOR SALE
DISTRIBUTION
NOT FOR SALE OR DISTRIBUTION
dence of paraplegia and organ ischemia/failure.
decrease acidosis, though it may be necessary to
As far as aortic cross-clamp time goes, a simple
give sodium bicarbonate as well. The surgeon may
rule
applies: Shorter is better. The duration of aorneed to remove the cross-clamp slowly to minimize
tic cross-clamping is directly related to the risk of
effects.
© Jones &these
Bartlett
Learning, LLC
© Jones
& Bartlett Learning, LLC
complications; cross-clamping the aorta for more
RenalOR
blood
flow decreases by 50% when the NOT
NOT FOR SALE
DISTRIBUTION
FOR
SALE OR DISTRIBUTION
than 30 minutes increases their incidence.
cross-clamp is removed. To compensate for this
effect, keep the patient hydrated and keep the BP
within normal limits.
Spinal Cord Protection During Aortic
Cross-Clamping
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& protected
Bartlett Learning,
LLC
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• The spinal cord ©
must
also be
from
Protective measures during aortic cross-clamping
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NOT
FOR
SALE
OR
DISTRIBUTION
severe hypotension after removing the aortic
aim to stabilize cell membranes, prevent release
cross-clamp by maintaining the BP within
of chemical mediators, and scavenge oxygen-free
normal limits.
radicals. These measures are summarized here:
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SPINAL
CORD
INJURY
AORTIC
NOT FOR
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OR AND
DISTRIBUTION
CROSS-CLAMPING
Spinal cord perfusion in the thoracolumbar area is
derived from the artery of Adamkiewicz (the prinarterial
supply of LLC
the anterior spinal cord). ©
&cipal
Bartlett
Learning,
© Jones
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• Thiopental
IV
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• Intrathecal
Papaverine
(3 mL OR
of 1%
strength)
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FOR SALE
DISTRIBUTION
• Corticosteroids (methylprednisone)
• Magnesium sulfate
• Mannitol
• Betablockers
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Chapter
3 Special
Techniques and Concepts
in Anesthesia
© Jones
& Bartlett Learning, LLC
© Jones20& Bartlett
Learning,
LLC
NOT
FOR
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NOT FOR SALE OR DISTRIBUTION
motor neurons in the anterior horn cells and is
• Drain 20–25 mL CSF prior to clamping to
more sensitive to ischemia.
decrease intrathecal pressure.
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Jones
Bartlett
LLC
© Jones & Bartlett Learning, LLC
• Maintain MAP
greater&than
70 mmLearning,
Hg
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NOT
FOR
SALE
OR
DISTRIBUTION
intraoperatively and postoperatively.
Aortic Shunt
Placement of a shunt may be used to bypass the
The MAP distal to the aortic clamp is decreased
cross-clamped aorta. In this case, the proximal end
and the distal spinal cord will be at risk of
of the shunt is placed in the ascending aorta and
ischemia. Several techniques can increase the dis© Jones & Bartlett Learning, LLC
Jones
& Bartlett
Learning,
LLC
the distal© end
in the
descending
thoracic aorta
tal arterial perfusion pressure, such as the placeNOT FOR SALE OR DISTRIBUTION
NOT
FOR
SALE
OR
DISTRIBUTION
past the aneurysm. Shunt flow should be approximent of a simple shunt (a shunt is placed above
mately 2.5 L/min, with distal MAP being maintained
and below the cross-clamp) or a partial (femoral
at more than 70 mm Hg.
vein to femoral artery) or full cardiopulmonary
Nevertheless, the spinal cord and kidneys canbypass (left atrium to femoral artery). Heparin is
© Jones & Bartlett Learning, LLC
© Jones
& Bartlett
Learning,
LLCwhen a shunt or
not
be
assumed to
be “protected”
given with these techniques.
NOT FOR SALEAdministration
OR DISTRIBUTION
NOT FOR
SALE
OREven
DISTRIBUTION
bypass
is used.
with these measures, atheroof nitroprusside can be detrisclerosis
may
prevent
significant
flow to the kidneys
mental to spinal cord perfusion by decreasing sysand spinal cord.
temic vascular resistance and shunting blood
Distal shunt placement advantages include the
away from the spinal cord vessels and collateral
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Jones
&
Bartlett
Learning,
LLC
© Jones
& Bartlett by
Learning, LLC
ability to attenuate proximal
hypertension
branches.
FOR via
SALE
OR DISTRIBUTION
NOT
SALEthe
OR
sending blood down pastNOT
the clamps
the shunt.
Cross-clamping
the FOR
aorta below
leftDISTRIBUTION
common
This approach may lead to perfusion of the vascucarotid increases the proximal systemic pressure,
lar beds distal to clamp. The placement of such a
which in turn increases the CSF pressure. This
shunt minimizes the risk of paraplegia, attenuates
increased CSF pressure can increase the incidence
metabolic
and
relieves Learning,
hypotension.LLC
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Jones
&
Bartlett
Learning,
LLC
©acidosis,
Jones &
Bartlett
of paraplegia and careful drainage of CSF can be
NOT
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beneficial.
BLOOD PRODUCTS
Spinal cord perfusion anterior spinal artery
pressure (SCPP)
pressure (distal aortic
MAP) CSF pressure
Whole blood: 500 mL. Contains red blood cells
(RBCs), plasma, white blood cells ( WBCs), and
along
with 63LLC
mL anticoagulant/
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© Jonesplatelets,
& Bartlett
Learning,
preservative.
Given
to
increase
NOT FOR SALEToOR
DISTRIBUTION
NOT FOR SALE OR DISTRIBUTIONred cell mass
increase
SCPP, either increase the distal aorand plasma volume.
tic MAP or lower the CSF pressure. SCPP should be
maintained at a level higher than 15 mm Hg.
Packed red blood cells (PRBCs): 300 mL.
Hypothermia at 32–24°C decreases spinal cord
Contains RBCs, WBCs, platelets, and some
© Jones
& Bartlett
Learning, LLC plasma. Each unit will
© Jones
& Bartlett
Learning, LLC
oxygen requirement,
decreases
tissue metabolism,
raise the
hematocrit
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FOR
SALE
OR
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FOR
SALE
OR
DISTRIBUTION
and increases tolerance to anoxia.
(HCT) by one third or hemoglobin (HGB) byDISTRIBUTION
It is important to prevent hyperglycemia when
1 g/dL. PRBCs are deficient in Factors V and VIII.
aortic cross-clamping is used. Maintain blood gluRBC washed: 175 mL. Has no plasma; has
cose levels between 80 and 120 mg/dL.
increased RBC mass; confers a reduced risk of
Prolonged
latency Learning,
or reduced LLC
amplitude of
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& Bartlett
© Jones & Bartlett Learning, LLC
allergy to plasma proteins.
SSEPsFOR
and MEPs
spinal cord ischemia,
NOT
SALEindicates
OR DISTRIBUTION
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although this relationship is not always reliable.
RBC leukocyte poor: 250 mL. Has no plasma;
SSEPs monitor sensory neurons in dorsal root
has increased RBC mass; confers a reduced risk
ganglia to the posterior column; MEPs monitor
of febrile reaction due to leukocyte antibodies.
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Carcinoid
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LLCSyndrome
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21
Platelets: 50 mL/unit. Don’t put on ice or heat,
CARCINOID SYNDROME
as such a temperature change affects platelet
Carcinoid syndrome refers to an array of symptoms
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Jones
& Bartlett
Learning,
LLC
© Jones & Bartlett Learning, LLC
function. Consists
platelets
and plasma;
each
that occur when a proliferation of cells secrete
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NOT
FOR
SALE
OR
DISTRIBUTION
unit will increase the platelet count by 7500
several vasoactive substances (e.g., serotonin,
to 10,000. Controls bleeding associated with
bradykinin, histamine, prostaglandins, and polypepdecreased platelet number or function.
tide hormones) from malignant carcinoid tumors.
These tumors arise from endocrine cells situated
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in the ileum, although they can also arise from anyFOR SALE
OR
DISTRIBUTION
where in theNOT
gastrointestinal
(GI)
tract,
pancreas,
gonads, or the bronchi. Serotonin release causes a
syndrome of episodic cutaneous flushing, diarrhea, bronchospasm, supraventricular dysrhyth© Jones
& Bartlett Learning,
LLCheart disease
mias, hyperglycemia,
and valvular
NOT
FOR
ORasthma.
DISTRIBUTION
and,
less SALE
commonly,
The current treatment of choice for significant
cardiovascular complications or bronchospasm
Fresh frozen plasma ( FFP): 200 mL. Must be
with suspected carcinoid syndrome is:
ABO compatible with the recipient’s RBCs; Rh
©
Jones
&
Bartlett
Learning,
LLC
© Jones & Bartlett Learning, LLC
matching need not be considered. FFP reverses
• Octreotide (Sandostatin) IV neutralizes serotonin,
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SALE OR
the effects of Coumadin
(warfarin).
FFPDISTRIBUTION
congastrin, insulin, glucagon, and vasoactive
tains all coagulation factors in normal amounts;
intestinal peptide (VIP). It is a universal inhibitor
it has no platelets, leukocytes, or RBCs. FFP is
of GI motility that acts by binding to somatostatin
made from plasma removed from a unit of
receptors in the GI tract.
©
Jones
& and
Bartlett
LLC
© Jones & Bartlett Learning, LLC
whole
blood
frozen;Learning,
it is not a concentrate
• Histamine (H1 and H2 ) blockers help the
NOT
FORfactors.
SALE One
OR DISTRIBUTION
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of clotting
unit of FFP increases
histamine-related symptoms.
clotting factors by 2%.
• Phenoxybenzamine and phenothiazines
control flushing from bradykinin release.
Cryoprecipitate: 15 mL/unit. Contains fibrino•
Glucocorticoids, indomethacin, and
gen F1, von Willebrand’s Factor VII, and fibrin
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Learning,
LLC
©
Jones
& Bartlett
Learning, LLC
nonsteroidal
anti-inflammatory
drugs (NSAIDs)
F13. Cryoprecipitate is given for hemophilia and
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OR
DISTRIBUTION
NOT
FOR
SALE
OR
DISTRIBUTION
inhibit
the
bradykinin
system
and
control
hypofibrinogenemia; it is also given to correct
flushing.
factor deficiencies. One bag contains 100 units
•
Aminophylline and steroids ease bronof Factor VIII and 250 mg of fibrinogen.
chospasm (secondary to bradykinin).
© Jones & Bartlett Learning,• LLC
© Jones
Bartlett Learning, LLC
Ondansetron can relieve nausea
and&diarrhea.
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NOT
FOR
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DISTRIBUTION
• Digitalis and diuretics may help with
Autologous blood does not need a filter.
congestive heart failure secondary to valve
Scavenged cell saver blood (BRAT) needs
malfunction.
a filter.
Platelets can use regular tubing or blood tubing.
Carcinoid Crisis
cryoprecipitate,
FFP can use
blood
©PRBC,
Jones
& Bartlettand
Learning,
LLC
© Jones & Bartlett Learning, LLC
tubing.
Carcinoid crisis
in patients
with 5-HIAA
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NOToccurs
FOR SALE
OR DISTRIBUTION
All products can be put through a fluid warmer
levels greater than 200mg/day and is precipitated
except platelets,
by stressful events (e.g., anesthesia, manipulation,
which should not be cooled or warmed.
chemotherapy, hepatic artery embolization). Patients
•© Jones
A male older
than age
18 can receive
& Bartlett
Learning,
LLC
any
Rh
and
type.
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• A female of child-bearing age must
receive Rh-appropriate platelets but
any type is acceptable.
•
A child
younger than
© Jones & Bartlett
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LLCage 18 must
an exact match in terms of Rh
NOT FOR SALEreceive
OR DISTRIBUTION
and type.
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Page 22
Chapter
3 Special
Techniques and Concepts
in Anesthesia
© Jones
& Bartlett Learning, LLC
© Jones22& Bartlett
Learning,
LLC
NOT
FOR
SALE OR DISTRIBUTION
NOT FOR SALE OR DISTRIBUTION
can experience flushing, severe abdominal pain,
systemic inflammatory response and activation of
explosive diarrhea, CNS depression, CV instability,
fibrinolysis; sternal wound infections; and respira© Jones
Bartlett
Learning,
& incidence
Bartlett Learning,
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profound hypotension,
CV &
collapse,
severe
hyper- LLC
tory insufficiency. There©isJones
a higher
of
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OR
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NOT
FOR
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OR
DISTRIBUTION
tension, tachycardia, and bronchospasm.
renal failure after CPB as the kidneys operate best
Treat carcinoid crisis with Octreotide 50–100 mcg
with pulsatile flow.
IV over 30 minutes, fluid resuscitation, and directacting vasopressors.
On-Pump Issues
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Surgical
Resection
Carcinoid
Tumor
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Cardiopulmonary
allows Learning,
the heart muscle
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to be still while the patient’s blood is diverted, oxygenated, and then reperfused. CPB can be either
Intraoperative management includes the following
total or partial. Three components of CPB are
measures:
hemodilution, hypothermia, and anticoagulation;
• Hydrate
the patient
well and consistently © Jones
© Jones & Bartlett
Learning,
LLC
& three
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• Monitor the CVP and urine output.
CPB must be established so that blood can be
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diverted from the body at the right atrium, the
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• Use succinylcholine with caution: It increases
Weaning off bypass may need to be gradual if
intra-abdominal pressure, but has been used
the patient’s blood pressure is too low. The perfusafely in these surgeries.
sionist will
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ing the heart
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is then decreased and ejection begins. It is also
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Postoperative treatment consists of chemotherown circulation along with bypass support) during
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to maintain partial CPB (parallel circuladitional coronary
graft (CABG)
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assess blood pressure and contractility, titrate volidentified, and cardiac stabilization devices were
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CEREBRAL
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ing blood product transfusion; aortic cannulation;
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Cerebral
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data suggest that this range is 70–150 mm Hg);
beneficial as thiopental. Furthermore, this agent is
vascular resistance changes in response to presmetabolized quickly, providing a more predictable
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See Chapter 9, Special NOT
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“Neuroauto regulation occurs in a higher MAP range) have
physiologic Monitoring,” for more information.
Fluid restriction is rarely used to lower ICP for
adapted to higher pressures and will not tolerate
purposes of cerebral protection, as it can cause
hypotension.
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Jones the
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Loop diuretics used for cerebral protection
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ing capacity.
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theLearning,
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Vasoconstrictor
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An osmotic diuretic, Mannitol 0.5–2 g/kg (or
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a free- Learning, LLC
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CMRO2 (cerebral metabolic
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and
will often order a specific amount in total to be
ICP. The cerebral metabolism reduction dose of
given, such as 50 g mannitol. (25% is 12.5 g in 50 mL)
thiopental is 4 mg/kg (2–5 g range dose). Pentothal
to be given over 15–30 minutes. Mannitol crystalis the only drug proven to save an ischemic brain.
lizes and should
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a filter nee© Jones &
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aminobutyric
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the N-methyl-D-aspartate receptor, thereby reducagent. Mannitol acts within 10–15 minutes and its
ing ischemic excitotoxicity.
effect last as long as 2 hours.
Propofol and etomidate are also potent cerebral
Mannitol can cause a triphasic hemodynamic
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Phase 1: transient (1–2 minutes) hypotension
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Chapter
3 Special
Techniques and Concepts
in Anesthesia
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© Jones24& Bartlett
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Mannitol can also have a biphasic effect on ICP:
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Phase 1: transient
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due to LLCCalcium-channel blockers
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such &
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nimodipine
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Lasix beforehand.
Interventions in Cerebral Protection
Phase 2: maximal reduction of ICP within
mnemonic
toBartlett
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cere© Jones
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10 minutes
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bral protection
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keep the head
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sists
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increases serum
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body temperature at 32°C.
across an intact blood—brain barrier ( BBB),
Carbon dioxide (hypercarbia) is a potent ceredrawing water out of the brain parenchyma.
bral&
vasodilator.
normal ETCO
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At
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imately 10%. CBF decreases 4% if the PaCO2
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Corticosteroids stabilize cell membranes, prevent
Hyperventilation is still the fastest way to
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decrease
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These agents
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vasoconstriction and reductions in CBF and CBV.
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tilation because CO2 crosses the BBB without limibefore the ICP is reduced, the advantage associated
tation. The effect may last only 6–8 hours before
with use of corticosteroids is that these agents
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the body’s balancing mechanisms kick in (metamay restore the BBB. Examples include Decadron
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bolic; bicarbonate levels change). One disadvan10 mg IV or methylprednisolone (also known as
tage of hyperventilation is that the decrease in CBF
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can cause ischemia in brain tissue.
While administration of steroids is useful in
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Hyperventilation
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glycemiaLearning,
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• Cerebral
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Insulin
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blood glucose to normoglycemic levels when corti• Increased pH decreases acidosis.
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Other pharmacologic methods of cerebral pro• Decreased brain bulk.© Jones & Bartlett Learning, LLC
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and good skeletal
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medication may also confer this kind of protection,
such as Dilantin (phenytoin) 1 gram IV piggyback
Hyperventilation should not be used in patients
drip. Give Dilantin very slowly as an IV medication,
with possible focal ischemia because of the “steal”
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sion and arrhythmias. Seizure activity produces
blood flow is increased in normal areas of the brain
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mal” energy demand.
A mild decrease in body temperature to 32–33°C
Magnesium may act as a free-radical scavenger;
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it may Learning,
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decreases
both basal
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and
Histamine
in the Operating
Room
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request; it is rarely used for cerebral protection
CMRO2 decreases 7% for every 1°C decrease in tempurposes (hypertension causes an increase in
perature. This is due to a reduction in the transJones
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means to decrease blood loss and hyperemic comwhich produces a neuron-sparing effect. To use
plications (cerebral edema or hemorrhage).
this approach to provide cerebral protection, pasGood oxygenation (hyperoxia) is based on the
sively expose patient to decrease body temperafollowing premises: A PaO2 less than 60 mm Hg
ture, or lay the patient on a cooling blanket but
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The condition
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Hypothermia can cause platelet dysfunction.
releasing free radicals and worsening neurologic
Blood viscosity can also be used to provide cereinjury. Studies show that a marked improvement in
bral protection. The optimal hematocrit range is
the survival of cortical neurons occurs if PaO2 kept
Anemia
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vides good oxygen-carrying capacity.
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Postural changes (i.e., raising the head of the bed
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up to approximately
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Keep the patient’s neck straight to facilitate venous
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outflow.
Deep hypothermic circulator y arrest (DHCA)
Planned CSF drainage from a ventricular catheter
for cerebral protection is discussed later in this
or lumbar
drain
can
also
be
used
to
protect
the
chapter.
© Jones & Bartlett Learning, LLC
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brain.
The
collection
device
is
placed
at
a
scale
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that allows for drainage. The drainage device is
COMMON ALLERGIES, ASTHMA, AND
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HISTAMINE IN THE OPERATING ROOM
CSF drains only when pressure is above that level.
Agents Associated with Anaphylaxis
A scale too high would impede drainage, whereas a
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choline, atracurium
Strict parameters of CSF removal, including
• #2 Latex
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• #3 Antibiotics: penicillin, cephalosporin,
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vancomycin
increased ICP, there is a chance the brain tissue
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•
#4 Colloids
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NOT propofol,
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• #5 Hypnotic/induction agents:
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Chapter
3 Special
Techniques and Concepts
in Anesthesia
© Jones
& Bartlett Learning, LLC
© Jones26& Bartlett
Learning,
LLC
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In addition to the cooling implemented by the
Histamine release from mast cells results in
perfusionist, the anesthetist packs the patient’s
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head in ice, over towels ©
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quate IV volume, or pretreatment with H1 or H2
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tions are extremely rare. Histamine release is asso© Jones
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The following
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itching,
andSALE
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Hypotension can
DHCA:
occur; it is especially likely to occur in a hypovolemic patient, in whom it may lead to orthostatic
• Right radial arterial line
hypotension. Nausea, vomiting, and retching due
• Right femoral arterial line
to stimulation
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trigger zone
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• Separate CVP line to monitor retrograde
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• Transesophageal echocardiography ( TEE)
Histamine blockers come in two varieties: H1
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Cerebral Protection with Hypothermic
Blood Flow
DEEP HYPOTHERMIC CARDIAC ARREST
Deep
hypothermic
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Antegrade Cerebral Perfusion
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ACP is a technique utilized to maintain selective
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surgery. The goal in using DHCA is to lower body
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temperature, thereby lowering the patient’s metaDHCA has been established, depending on the
bolic rate and oxygen demand to the point where
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stopped for an extended period of 45–60 minutes.
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monary bypass is established. Pharmacologic cererograde perfusion catheters are then placed into
bral protection is implemented prior to initiating
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and directly into the left carotid; these catheters
The perfusionist decreases the core body temare attached to individual pump heads on the CPB
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perature to 14–18°C; that temperature is maintained
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until approximately 20 minutes prior to circulatory
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fused with cold blood while the patient is mainwith minimal cerebral complications is approxitained in DHCA. Distal and arch vessels are
mately 45 minutes at 18°C and 1 hour at 15°C.
anastomosed to the replacement aortic tube graft;
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Deep Hypothermic
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delivery is not reliable, as only 20–60% of the brain
ACP is terminated and the balloon catheters are
is perfused with retrograde flow; ability of venous
deflated and removed. The new graft is flushed and
© blood
Jonesflow
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valves
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divert the flow; and ability of drainage from the RCP
cannula. Once the new graft is de-aired, total body
catheter to affect the surgical view.
perfusion is reinitiated and rewarming begins.
ACP has several notable advantages. For example, cerebral flow provides uniform cooling in a norAnesthesia Considerations with DHCA
Jones
& Bartlett
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mal©
flow
direction,
and metabolic
substrate
delivery
• Prolonged effect of anesthesia agents due to
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tends
to have
favorable
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slowed drug metabolism and elimination
also been shown to be a more effective cerebral pro• Decreased minimal alveolar concentration
tector than retrograde flow. Disadvantages include
(MAC) of inhalational agents
the complexity of the procedure, the presence of an
• Need for a narcotic, amnestic, and nondepolarcannula
on the surgical
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patient
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ficulty level of performing this procedure.
• Positioning and padding must be meticulous
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to nerve and tissue injury
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RCP, with deep hypothermic
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Monitor urine output every
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increase the safe arrest
to the
report it to the perfusionist
fragility of the venous system (compared to the arterial system), RCP is maintained at a pressure of
Surgical Considerations with DHCA
20–25 mm Hg at 8–14°C (flow rates depend on presDHCA provides for a bloodless field. There is also
sures
are usually
approximately
500–800
mL/min).
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no need for aortic cross-clamping, thereby reducing
TheNOT
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the risks associated with embolization sequelae.
tion to ensure brain perfusion.
After DHCA is initiated, the arterial perfusion
Systemic Effects from DHCA
line is connected to the SVC cannula and low perflow is initiated backward or retrograde
Cerebral
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through the brain. The brain is perfused in retro• Rapid core cooling to 15–18°C. EEG becomes
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grade fashion with cold, oxygen-rich blood with
flat at 18°C.
100% oxygen saturation via SVC to jugular vein; the
• Protection with metabolic suppression occurs
blood will come back through the carotid and
by severe reduction of body temperature,
innominate arteries and is recovered by suction.
reducing intracellular enzymatic reactions and
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Advantages of RCP include effective global cerethereby reducing oxygen demand and cerebral
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bral cooling; decreased cerebral embolization;
blood flow.
ability to wash out air bubbles, embolic debris,
• Fewer cerebral intracellular enzymatic
and metabolic waste products; use of simpler sysreactions.
tem; avoidance of fragile vessels; and delivery of
• Proportionate reduction in cerebral oxygen
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oxygen and nutritional substrates to brain tissue.
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Moreover, use of RCP decreases strokes and neuro• Brain tissue protectant—preserves pH and
logic injury.
ATP stores.
Disadvantages of RCP include increased cerebral
• Decreased cerebral oxygen consumption. The
edema from over-perfusion; the fact that substrate
patient is able to tolerate anoxia longer.
Retrograde Cerebral Perfusion
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Chapter
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• Edema, which can occur after hypothermia
increased viscosity of the patient’s blood at
due to cellular membrane permeability.
these extremely cold temperatures, which also
©EEG
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• An isoelectric
and bispectral
analysis
perfusion.
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• Cerebral macro-circulatory obstruction
monitor (BIS) reading of 0—used to gauge the
rence from coagulopathy.
degree of hypothermia necessary to prevent
• Impaired enzymatic activity of clotting factors,
neurologic damage. Different areas of the brain
promoting abnormal clot formation; a slowed
have varying abilities to tolerate a lack of
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cascade;
decreased
platelet LLC
oxygen: &
Some
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short
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number
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DHCA
to
ischemic
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greater blood product requirements.
function for longer periods under these
• Decreased heparin metabolism.
conditions. The amount of time the brain can
• Hyperglycemia: Requires monitoring of glucose
tolerate ischemia depends on its tissue energy
maintain
between 80–120
stores
and the rate
of energy consumption. © Joneslevels,
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& Bartlett
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ORrate
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temperature, metabolic rate, brain activity, and
Metabolic Effects
the use of anesthetics.
• Change of 1°C 7% metabolic decrease.
• Hypothermia: CMRO2 is decreased by approxi• Carbon dioxide production—decreased due to
mately 7% per
decrease
in temperature.
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rate. CO&2 levels
A mild body NOT
temperature
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should be adjusted toNOT
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a PaCO
2 of
is most effective; it decreases both basal and
40 mm Hg to help prevent cerebral injury.
metabolic requirements.
• Metabolic acidosis due to peripheral hypoper• Blood viscosity: Optimal hematocrit is 30–35.
fusion; increased production of lactic acid with
• Jones
Injection&ofBartlett
Papaverine
into subdural
cold body
temperature.
ETCOLearning,
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2 levels will rise
can
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to
dilate
the
anterior
spinal
artery
with the
reperfusion
after OR
blood
flow is
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restored.
Cardiovascular Effects
DOUBLE-LUMEN ENDOBRONCHIAL TUBE
• Oxyhemoglobin dissociation curve: shifts
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One-lung ventilation allows for the collapse of the
the left with oxygen less readily available
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operative lung; it facilitates surgical exposure. With
•
•
•
•
to the tissues. The reduced oxygen demand
a double-lumen endobronchial tube (DLEBT), the
from core cooling usually mitigates this
following settings are used:
effect.
Decreased heart rate.
• Proximal tracheal cuff:©10–20
mL &
airBartlett
(high
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Jones
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Increased SVR with decreased cardiac output
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and decreased LV compliance.
• Bronchial cuff: 3 mL only
Prolonged refractory period.
The tube and stylet should be coated liberally with
Heart: most susceptible to ventricular fibrillaa water-soluble lubricant (or spray).
tion when the body is warmed to 30°C.
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Hematological Effects
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DLEBT Sizing in Adult Patients
• Coagulopathy from the profound cooling—due
• Height of 170 cm (approximately 5 feet,
to clotting factor and platelet dysfunction and
5 inches): 29 cm at central incisors; advance or
activation (of platelets) with release of
withdraw the tube by 1 cm for each 10-cm
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granules. Hemodilution is needed to prevent
height difference.
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Double-Lumen
Endobronchial
Tube
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29
165 cm (less than 5 feet, 3 inches): 35–37 Fr
• Females: typically use DLEBT 35–39; place the
largest device you can to decrease resistance
165–179 cm (5 feet,
3 inches&toBartlett
5 feet, 8 inches):
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Males: typically use DLEBT
39–43 & Bartlett Learning, LLC
37–39 Fr
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179 cm (greater than 5 feet, 8 inches): 39–41 Fr
DLEBT Sizing in Pediatric Patients
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1 y LLC
2y
3y
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4y
kg
1.5
3.5
7
10
12
14
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lb
3.5
7.5
15
22
26
31
37
5y
6©
y
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y
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20
40
44
49
25
33
40
55
73
88
50
DLEBT
size
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26 26–28LLC
32
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35
• Deliver continuous positive airway pressure
For all patients, it is important to remove the
(CPAP) on the deflated lung (surgical lung).
stylet before rotating and advancing the DLEBT to
• Deliver positive end-expiratory pressure
avoid tracheal or bronchial lacerations. Once the
(PEEP) on the inflated lung.
tube is thought to be
the tracheal
© placed
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& Bartlett
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• Jet ventilation may be helpful
low
drivingOR DISTRIBUTION
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ventilation
of
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pressure and an increased respiratory rate.
both lungs established. (Is it through the vocal
• Allow the patient to desaturate to a certain
cords and in trachea?)
level, have the surgeon stop the procedure,
To check for proper position, go into the trainflate both
lungs and
the patient to
cheal
lumen first.
In pediatric
patients, LLC
use a pedi© Jones
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& oxygenate
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the
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and
then
clamp
lung
again
atricNOT
flexible
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(until the patient desaturates again).
Obtain a baseline ABG on two-lung ventilation;
• Band the pulmonary artery (PA) to stop blood
remeasure ABG after 15 minutes on one-lung
flow to the surgical lung. This step can be
ventilation.
taken only if the surgical team is performing a
When going from two-lung to one-lung ventilation:
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total pneumonectomy.
Go toOR
100%
FiO2.
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• Decrease the tidal volume.
Indications and Contraindications for DLEBT
• Increase the respiratory rate.
Absolute indications (to isolate one lung from
• Clamp the tube to the non-dependent lung.
the other): Infection, massive hemorrhage,
• Open the pop-cap
the air.& Bartlett Learning, LLC
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thanDISTRIBUTION
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In case of decreasing SaO2 with DLEBT with
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surgery ( VATS) requires lung separation and is
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becoming
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Relative Indications: Surgical exposure for tho• Administer 100% FiO2.
racic aortic aneurysm; pneumonectomy; upper,
• Check tube position and make sure the cuff
middle, or lower lobectomy; or esophageal
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Chapter
3 Special
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Contraindications: Airway lesion, poor laryngeal
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would &
be Bartlett
life-threatening.
• Open sinuses.
• Open, large veins.
LLC
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• Cement impaction in ©
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when air is forced into vessels.
EMBOLISM
• Sitting position.
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Venous Air Embolism
surgery is dealing with highly vascular
Air embolism is the abnormal presence of air or
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membranes;
e.g.,&the
dura canLearning,
entrain air LLC
carbon
dioxide
in the vena
cava andLLC
right atrium,
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when
cut.).
resulting in obstruction of the flow of blood
• Low central venous pressures (especially from
through the heart. Venous air embolism (VAE) is
positioning the legs too low)
related to a mass of foamy bubbles that interfere
• Inadvertent opening of a large-bore venous
with the right heart venous outflow tract; blood
catheter
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cannot get into the heart (venous return) and,
• Accidental
IV bolus
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therefore,
cannot get into the lungs because ofNOT
all FOR
•
Traumatically,
as
by
a puncture wound
the air. Cardiac output will fall and circulatory collapse may result. One-third of 1 mL air can cause
Nitrous oxide can markedly accentuate the effects
problems; 50 mL air is lethal. The latter condition
of even small amounts of air.
©heart
Jones
Bartlett
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causes air lock in
(air&
cannot
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into lungs) LLC
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accompanied byNOT
a foamy,
incompressible
mass.
Monitors for VAE
The physiologic consequences of VAE depend
The monitors for VAE are presented here in order
on the volume of air, the rate of air entry, and the
of decreasing sensitivity.
presence or absence of a patent foramen ovale
(PFO).
A PFO
can facilitate
passage of
air into arteTransesophageal
echocardiography
©
Jones
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© Jones & Bartlett
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LLC):
rial circulation
(paradoxical
air embolism), espeTransesophageal
echocardioNOT
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cially when the normal transatrial (left→right)
graphy is the most sensitive intraoperative
pressure gradient is reversed. Reversal of this gramonitor but some consider it “too sensitive”
dient is favored by hypovolemia and perhaps by
due to the potential for false positives. TEE
PEEP. Potential
end-organ
every Learning,
bubble. Some
argue though that
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LLC damage can also occur
© Jones“sees”
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from
paradoxical
air
emboli
to
the
microvascular
detecting
even
small
amounts
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circulation.
embolism is important because it allows surgiVAE can occur when the pressure within an open
cal control of the entry site before additional
vein is subatmospheric. This pressure gradient
air is entrained. TEE has the added benefits of
develops when the surgical site is higher than the
detecting the amount of bubbles and their
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right atrium (approximately 2-torr pressure differtransatrial passage, as well as evaluating carNOT FOR SALE OR DISTRIBUTION
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ence for 1-inch difference in height). These condidiac function. TEE is expensive and requires
tions may exist in any position (and during any
trained personnel to be continually available
procedure) whenever the wound is above the level
for interpretation. There is also potential for
of the heart:
injury to the esophagus or larynx; there have
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been reports of esophageal rupture and recur• Sitting
craniotomies
incidence of VAE,
NOT
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rent laryngeal nerve injury with TEE use.
at 25–50%), especially with open bone.
• Severe barotrauma associated with mechanical
Precordial Doppler: The monitor is placed
ventilation.
over the right atrium ventricle at the second
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31
through sixth intercostal spaces at the right
• The surgeon will flood the surgical field with
sternal border. Interruption of regular swishing
normal saline and apply bone wax.
Jonesby& sporadic
Bartlett Learning,
© Jones
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of the Doppler© signal
roaring
•LLC
Aspirate the central venous
line/PA line
in an
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sounds or a high-pitched whoosh (called millattempt to retrieve the entrained air. Note that
wheel murmur) indicates venous embolism.
the aspirate may appear foamy.
Even 0.25–0.5 mL of air can be detected.
• Occlude the neck veins; discontinue pressurPrecordial Doppler is considered the best air
ized gas.
© Jones monitor,
& Bartlett
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LLC but • Place the©patient
Jones
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embolism
because
it is sensitive
in steep
Trendelenburg
or left
NOTnot
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ORofDISTRIBUTION
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does
generate
false positives.
lateral position.
• Vasopressors should be given to correct
ETCO2 monitoring: A sudden decrease in
hypotension.
expired carbon dioxide may indicate VAE.
• Give intravascular volume infusion to increase
central
venous pressure.
© Jones &Signs
Bartlett
Learning,
LLC
©
Jones
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of VAE
• FOR
Use PEEP/CPAP
toDISTRIBUTION
increase CVP (although
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following
signs also have air emboli as a differ- NOT
there
are
some
arguments
against doing this).
ential diagnosis. These signs can occur with anaphy• Undertake cardiopulmonary resuscitation, if
laxis, acute myocardial infarction, and pulmonary
necessary.
embolism.
© Jones & Bartlett Learning, LLC
© Jones & Bartlett Learning, LLC
Sudden hypotension
Prevention of VAE
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Decreased SaO2/PaO2
Prevent hydrostatic gradient development by limitChange in heart sounds, cardiac murmur
ing positions where the operative site is above the
EKG changes and dysrhythmias; tachycardia
right atrium. Maintain vigilance for VAE in high-risk
Sudden decrease in expired carbon dioxide
situations.
©
Jones
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© Jones & Bartlett Learning, LLC
(ETCO
2 ): decreases due to a fall in cardiac
NOT
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outputFOR
and increased
dead
space
Carbon Dioxide Gas Embolism
• Appearance of nitrogen in the expired gas
There is a risk of carbon dioxide embolus during a
• Increased pulmonary artery pressure (PAP)
laparoscopic procedure; gas may enter the circulaand central venous pressure (CVP)
tion through any opening in an injured vessel. This
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Sudden Learning,
appearance of
vigorous spontaneous © Jones
type of embolism is the most dangerous complicaNOT FOR SALE
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ventilation despite continuing mechanical
tion associated with laparoscopy. It develops prinventilation
cipally during induction of a pneumoperitoneum.
•
•
•
•
•
With carbon dioxide embolus, “gas lock” occurs in
Signs of VAE are often not apparent until large
the vena cava and right atrium; venous return is
amounts of air have been entrained. Rapid entrain©
Jones
&
Bartlett
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Jones
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obstructed.
Blood cannot ©go
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ment of large amounts of air can produce sudden
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artery. Cardiac output will fall and circulatory
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lapse may result.
outflow.
Treatment of VAE
Signs of Gas Embolism
• ©
Inform
everyone.
Jones
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• NOT
Immediately
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and release the
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• Hyperventilate with 100% oxygen; discontinue
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Signs of carbon
dioxide&embolus
include
a sudden
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;
ETCO
decrease in NOT
expiredFOR
carbon
dioxide
SALE
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2
decreases due to the fall in cardiac output and
increased dead space), unexplained tachycardia,
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Chapter
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increased PAP and CVP, a change in heart sounds,
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2.
Lungs
• Dyspnea
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Treatment of Gas Embolism
• Immediately cease insufflation and release the
pneumoperitoneum.
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• Position&the
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• Hyperventilate with 100% O2.
• Aspirate gas if a CVP catheter is in place.
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• Decreased PaO2 and oxygen saturation
• Decreased ETCO2 and arterial hypoxemia
• ARDS (interstitial edema, alveolar collapse,
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Neurological
• Level of consciousness (LOC) changes
• Confusion
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•
Seizures
Fat
Embolism
Syndrome
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• Coma
Fat embolism syndrome ( FES) is a rare clinical
condition in which embolized and circulating fat
particles are deposited in the pulmonary capillary
Heart
beds and brain©tissue
and
to multisystem
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& lead
Bartlett
Learning, LLC
© Jones
& Bartlett Learning, LLC
• EKG changes (dysrhythmias,
tachycardia,
dysfunction in the
skin,
lungs,
blood,
and
brain.
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ischemic changes) NOT FOR SALE OR DISTRIBUTION
Microvascular plugging of these fat droplets produces local ischemia, causing the release of inflamBlood
matory mediators and platelet aggregation.
• Thrombocytopenia
Implicated
procedures
and causes
include long
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LLC
© Jones & Bartlett Learning, LLC
• Anemia
bone
fractures,
multiple
fractures
with
pelvic
injury,
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• Coagulopathy
total joint replacement, intra-abdominal surgery,
• Disseminated intravascular coagulation (DIC)
liposuction, bone marrow transplant, and burns.
• Increased lipase
A factor increasing the risk of FES is aggressive
• Triglyceride levels
reaming or nailing of the bone’s medullary cavity.
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• Fat
globules in
urine and sputum
Mobilized fat particles occur to some degree in
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OR
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OR
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• Decreased serum calcium levels (calcium
most long bone fractures.
binds with free fatty acids)
Symptoms may be subclinical or masked by
general anesthesia; manifestations of FES may
occur 12–72 hours after injury.
Diagnostic Tests for FES
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© Jones & Bartlett Learning, LLC
• Fat globules in urine and sputum
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Signs and Symptoms of FES
FES has three main symptoms: dyspnea, confusion,
and petechiae. All together, the following signs can
be seen with FES:
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Skin
• Petechiae (transient cutaneous pin-point sized
red dots in the axilla, conjunctiva, neck, shoulders, chest, arms)
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• Complete blood count: anemia and
thrombocytopenia
• Increased lipase and triglyceride levels
• Low calcium levels (calcium binds with free
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fatty acids)
Supportive Measures for FES
• Adequate hydration
• Oxygenation
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High-Frequency
Jet Ventilation
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• Early splinting of fracture especially long bones
• Give albumin to provide free fatty acid
binding sites © Jones & Bartlett Learning,
33
• Extremely high cpm: 400 cpm may
decrease inspiratory time (worsens CO2
LLC elimination)
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High-dose steroids have not been proved effective for
treatment of FES.
Tidal volume ( VT) less than dead space
(2–5 mL/kg)
HEMODIALYSIS
CATHETER
ACCESS
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AND
FLUSH
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CO2 eliminated by passive expirations
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Jones
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through an
system/exhalation
takes place
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continuously
This section outlines the authors’ practice policy
and is just one example of dialysis catheter access
guidelines. Check your institution’s policy for your
guidelines.
&specific
Bartlett
Learning, LLC
©
© Jones
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A physician’s
order must be written on the
ETT with special connector; attaches to any
tube with a 15-mm connector
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Factors Affecting Ventilation during HFJV
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Driving Pressure
chart before the provider can access a dialysis
Driving pressure (DP) is measured in pounds/
catheter.
square inch (psi). It is the pressure of the force of
• Use a dialysis catheter only if you are unable to
2O/O
2 (not&inhalation
© Jones
& Bartlett Learning,inhaled
LLC gases: air/O2 or N©
Jones
Bartlett Learning, LLC
get any other vascular
access.
agents). In the Venturi effect, velocity of airflow
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NOTwhen
FOR
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OR DISTRIBUTION
• Use sterile technique
accessing
ports!
increases through a small orifice, resulting in a
• Wear sterile gloves and clean the ports using
decreased pressure; this effect causes a decrease
sterile technique. Cleanse with Betadine soluin the pressure at the outflow of the jet injector,
tion for 30 seconds on the caps. Aspirate out
and gas will be entrained, increasing the tidal voltheJones
heparin&flush
and discard
it; flush
the port
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Bartlett
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© Jones & Bartlett Learning, LLC
ume at 10–20%. This volume must be humidified
with normal
saline ( OR
NS); DISTRIBUTION
and connect the port
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for cases where surgery lasts more than 45 minutes
to the NS fluids.
or in ICUs.
• Have the circulator order heparin 5000 units/mL
from the pharmacy so you will have it ready. If
Percent Inspiratory Time with HFJV
the dialysis
catheter is
not your only access,
© Jones & Bartlett
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LLC
© Jones
& Bartlett
Learning,
LLC ratio (I:E)
Increasing
the inspiratory
to expiratory
then OR
you should
discontinue IV fluids in the OR NOT FOR SALE OR DISTRIBUTION
NOT FOR SALE
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ratio will increase tidal volume and minute ventilaand flush with the previously described heparin
tion. The range is usually set between 30% and
solution. If this catheter is your only access,
50%. Minute ventilation is most dependent on DP
then take the heparin with you; the hemodialyand the I:E ratio.
sis catheter can be flushed in the PACU.
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© Jones & Bartlett Learning, LLC
Jet Catheter Size and Configuration
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HIGH-FREQUENCY JET VENTILATION
The bigger the catheter, the greater the jet volume
There is no bulk flow of gases with high-frequency
jet ventilation (HFJV); it is referred to as coaxial
flow
the larger
airways. Learning,
Following are
the usual
©inJones
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LLC
setting
ranges
for
HFJV:
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Rate 60–600 cycles per minute (cpm)
• Lower cpm: 60 cpm will increase inspiratory time (improves CO2 elimination)
© Jones & Bartlett Learning, LLC
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and minute ventilation. It is best to have two side
holes for entrained volume: jet velocity or tip
velocity from
nozzle.
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Cycle Rates
Generally, changing the cycle rate does not change
minute ventilation. The exception occurs when
delivering
HFJV at rates
60 cpm
and 400 cpm.
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Chapter
3 Special
Techniques and Concepts
in Anesthesia
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NOT
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FiO2
patient becomes severely bradycardic; team members can decrease insufflation pressures a little or
The FiO2 percent used is a matter of choice and
© Jones & Bartlett Learning, LLC
Jones
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completely until the heart©
rate
increases.
IV glycopydepends on the case and technique employed.
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rrolate may need to be given to increase the heartDISTRIBUTION
Blenders are used for O2, air, or N2O.
rate. If glycopyrrolate is ineffective, IV atropine
should be given. Have epinephrine 1:10,000 immediHumidity
ately available for severe bradycardia unresponsive
Humidity can be delivered using a small saline bag
© Jones
& line
Bartlett
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LLC The rec- to vagolytics
© Jones
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medications.
and
infusion
with some
ventilators.
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FORgases
SALE
ORincrease
DISTRIBUTION
CarbonNOT
dioxide
can
end-tidal
ommended
is 15
cc/h
0.9% NS or 0.45% NS.
carbon dioxide (ETCO2 ) but should level out after
This technique may not be used in the OR; it is
30–45 minutes. This increase can be offset by
associated with fog buildup if the surgeon is workincreasing the minute ventilations to keep the
ing with airway scopes.
ETCO
in appropriate
rangesLLC
(32–39 mm Hg). If
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© Jones
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LAPAROSCOPIC
ISSUES
ETCOSALE
rise, check for subcutaneous
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NOT FOR
OR to
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2 continues
Laparoscopic surgery involves the introduction of
emphysema; the insufflation pressure may need to
a laparoscope through a single or multiple ports
be reduced and ventilation increased dramatically.
placed through a body wall into a cavity. Usually
Once pneumoperitoneum is achieved, setting
several 2- to 3-cm
slits are&made
across
the skin LLC
the ventilator on pressure-controlled
ventilations
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Bartlett
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surface where NOT
portsFOR
are SALE
placed,
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can
help
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pressures
while
mainNOT FOR SALE OR DISTRIBUTION
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retrieved, and surgery performed. Laparoscopic
taining oxygenation, lung expansion, and ETCO2
surgery is done for exploration, diagnosis, and
while the pneumoperitoneum lasts. Tidal voltreatment purposes. To visualize an internal surumes may need to be decreased to allow adeface,
the
external
body
surface
is
distended
away
quate pneumoperitoneum.
The Learning,
anesthetist LLC
must
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from the internal organs by establishing insufflabe constantly
of the presence
of the pneuNOT
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NOT aware
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tion with carbon dioxide.
moperitoneum. The surgeon may decrease or
With abdominal laparoscopy, the parietal wall is
desufflate at any time; if the ventilator is set on
distended away from the internal organs by estabpressure ventilation and the pneumoperitoneum
lishing a pneumoperitoneum with CO2. Before
is lost, the patient’s lung volumes may increase
© Jones & Bartlett
Learning, LLC
© Jones
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insufflating the area, the anesthetist inserts an
dramatically.
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OR
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NOT
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orogastric or nasogastric tube and suctions out the
The patient may be moved from Trendelenburg
stomach contents. A urethral catheter should also
position to reverse Trendelenburg position several
be placed by the OR staff.
times during surgery to change internal organ posiWhen the trocar pierces a body cavity, the anestioning so as to facilitate organ exposure for sur©
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&
Bartlett
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thetist should monitor viewing screens to look for
geon. If the patient’s arms
secured
on padded
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OR
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any internal trauma (i.e., the trocar piercing an
armboards, be sure to secure both the forearm andDISTRIBUTION
internal organ).
the upper arm to eliminate the chance of the arms
Insufflation pressures used are usually between
rolling off the boards.
5 mm Hg and 14–16 mm Hg and can decrease cardiac
Urine output tends to diminish with insufflation
©
Jones
& Bartlett
LLCfunctional of the abdomen.
© JonesNausea
& Bartlett
Learning,
output,
venous
return, Learning,
and the lung’s
and vomiting
are LLC
more
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residual capacity (FRC). Increased abdominal prescommon following laparoscopic procedures.
sure from insufflation can also stimulate vagal nerve
Patients may complain of right shoulder/
activity, and the patient’s heart rate can become
shoulder blade pain after a laparoscopic surgery.
bradycardic to asystolic. Notify the surgeon if the
This effect is thought to be due to carbon dioxide
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© Jones & Bartlett Learning, LLC
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(Ventilator)
StrapLLC
Facial Injuries
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Bartlett
Learning,
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35
insufflation causing chemical irritation to the
Pneumothorax
diaphragm.
Pneumothorax may occur due to a defect in the
& Bartlett
Learning,diaphragm
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Jones
& IfBartlett
Carbon dioxide ©
gasJones
embolism,
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or as a result of a©
pleural
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pneumomediastinum, subcutaneous emphysema,
of preexisting bullae occurs in the lung, causing
and hypercarbia with ensuing acidosis are potenair to escape into the thorax, the pneumothorax
tial risks of CO2 insufflation. Air can enter the thowill not resolve spontaneously. A thoracentesis
rax through weakened areas in the diaphragm.
(pleural tap) must be done to remove the air in
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& Bartlett
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Jones
& Bartlett(carbon
Learning,
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Immediate
chest
tube decompression
required
the pleural ©
space.
Capnothorax
dioxide
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for any
clinical
a tension
pneumothorax.
in the pleural space) without pulmonary trauma
Effects of Abdominal Laparoscopic Surgery on
the Respiratory System
will spontaneously resolve 30–60 minutes after
ex-sufflation. Treatment of CO2 or venous air pneumothorax consists of adding PEEP and reducing all
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intra-abdominal
pressure.
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of CO2 creates a pneu- ©
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that results in ventilatory and res- NOT FOR SALE OR DISTRIBUTION
piratory changes:
Carbon Dioxide Gas Embolism
See the discussion of this condition presented ear• Decreases thoraco-pulmonary compliance.
lier in this chapter.
• Decreases lung compliance by 30–50%.
© Jones & Bartlett Learning, LLC
© Jones & Bartlett Learning, LLC
• During uneventful laparoscopy, PaCO2
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NOT FOR SALE OR DISTRIBUTION
CO2-Subcutaneous Emphysema
progressively increases and reaches a plateau
This condition develops secondary to extraperi15–30 minutes after insufflation. The increase
toneal insufflation. It results in increased carbon dioxin PaCO2 depends on the intra-abdominal
ide levels after ETCO2 has plateaued. Hypercapnia
pressure.
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& adjustment
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becomes unresponsive
of ventilation.
• Once the pneumoperitoneum is created and
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To resolve this
laparoscopy
should be
kept constant, compliance is not affected by
temporarily
interrupted
to
allow
for
CO
elimination.
patient tilting or changes in minute ventilation.
2
Respiratory Complications from Abdominal
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Intubation
MASK &
(VENTILATOR)
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FACIAL
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Direct pressure on the patient’s brow from the
Cephalad displacement of the diaphragm during
ventilator face mask can cause hair loss or nerve
pneumoperitoneum also results in cephalad movedamage. The facial nerve can also be affected,
ment of the carina; this effect may occur even in
specifically
at the following branches
Bartlett
LLC
© Jones(all
&branches
Bartlett Learning, LLC
laparoscopic cases©inJones
which &
the
patient Learning,
is in a
are listed):
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head-up position. If the patient’s oxygen saturation
decreases after insufflation of the abdomen, check
• Temporal branch. Supraorbital pressure, espefor bilateral breath sounds. The tracheal tube can
cially by the ETT connector, can cause eye
go into the right mainstem bronchus, with the
pain, photophobia, and/or forehead numbness.
© Jones
& Bartlettpushing
Learning,
© branch.
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pressure
of insufflation
the LLC
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• Zygomatic
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upward. If breath sounds are decreased on the left
• Buccal branch.FOR
This branch
the
side, pull the endotracheal tube back until breath
orbicularis oris around the mouth; damage to
sounds are audible bilaterally and retape the endothis branch can cause loss of motor ability
tracheal tube.
(e.g., no puckering of lips).
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Chapter
3 Special
Techniques and Concepts
in Anesthesia
© Jones
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© Jones36& Bartlett
Learning,
LLC
NOT
FOR
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• Mandibular branch. Damage to this branch can
petechiae on the neck, shoulders, and
cause motor loss and minimal sensory loss to
chest.
© Jones & Bartlett Learning, LLC ■ Treatment: supportive,
© Jones
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the mandible.
oxygenations,
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• Cervical branch.
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bones.OR DISTRIBUTION
• Ambient contamination: fumes
■
MMA should be mixed in a vented hood.
METHYLMETHACRYLATE BONE CEMENT
■
Liquid monomer is highly flammable.
Methylmethacrylate
(MMA)
is
a
self-polymerizing
■
© Jones & Bartlett Learning, LLC
© Jones
&and
Bartlett
Learning,
LLC
Contact
lenses
other plastics
can be
bone
that isOR
used
to secure a prosthesis
NOT cement
FOR SALE
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NOT by
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affected
MMA
vapors.
inside the bone/joint. It is part of an exothermic
■
Vapors can cause irritation of the eyes and
reaction that leads to cement hardening and expanrespiratory tract.
sion against prosthetic components. This expan• Mortality
sion can exert pressure in excess of 500 mm Hg in
canLearning,
occur intraoperatively
or post© Jones & Bartlett
Learning, LLC
© Jones■& Deaths
Bartlett
LLC
the intramedullary space. MMA can embolize fat,
operatively
due to pulmonary embolism.
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clot, air, cement, marrow, and bone chips. Its reac■
PE may result from the impact from
tion may also trigger tissue thromboplastin, caussurgical instrumentation and the
ing small clots to travel to the lung. Unpolymerized
expansion/pressure of the cement against
monomer can be absorbed into the circulation.
© Jones & Bartlett Learning, LLC the femoral shaft. © Jones & Bartlett Learning, LLC
Pressurization of the bone canal with cement is
NOT
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ORinDISTRIBUTION
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MMA use can also cause
significant
increases
also associated with hemodynamic changes.
PVR and pulmonary wedge pressure and decreases
in SVR, CO, and MAP pressures. Hypotension, hypoxia,
Complications of MMA Use
cardiovascular collapse and arrest, and pulmonary
The
following
problems
are associated
with
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Jones
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Jones prosthesis
& Bartlettinsertion
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embolus ©
following
have LLC
been
MMA use:
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reported.NOT FOR SALE OR DISTRIBUTION
• Hypotension
Prevention of MMA-Related Complications
■
MMA may be a direct vasodilator/
• Better surgical lavage helps to avoid
myocardial depressant.
■
Severity:
usually
related to volume (could© Jonescomplications.
© Jones & Bartlett
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• Maintain
for potential problems.
result
from a pulmonary embolism [PE] or
NOT FOR SALE OR
DISTRIBUTION
NOT FOR
SALEvigilance
OR DISTRIBUTION
• Use 100% oxygen (FiO2 ) when using MMA.
anaphylactoid reaction).
■
Onset: 30 seconds to 10 minutes.
MIXED VENOUS OXYGEN CONTENT
■
Termination: usually spontaneous within
Mixed venous oxygen content
(MVO&
also known
5 minutes.© Jones & Bartlett Learning, LLC
© Jones
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2 ), Bartlett
■
Treatment:
adequate
to full
as saturated venous oxygen
content
),
is
an
NOT
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2
support.
index of cardiac output and overall tissue perfu• Desaturation
sion. Its ongoing measurement allows minute-to■
Result: In one study, 34% patients had
minute assessment of total tissue oxygen balance
desaturation
withLearning,
a baseline FiO
(delivery©versus
consumption)
the tissue level.
2 of 33%.
© Jones
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Jones
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■
Treatment:
increase
FiO
to
at
least
50%
MVO
varies
directly
with
cardiac
output, hemo2
2 NOT FOR SALE OR DISTRIBUTION
NOT FOR SALE OR DISTRIBUTION
during cementing.
globin levels, and oxygen saturation. It varies
• Fat embolism
inversely with tissue oxygen requirements and oxy■
Result: arterial hypoxemia, ADRS, coagugen consumption (VO2 ). Normal MVO2 is considlopathy, fever confusion, coma, seizures;
ered to be in the range of 65–75%; 25% extracted
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Electro Encephalography
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37
and utilized in body tissues. In other words, under
monitor the effects of anesthetic agents and other
CNS drugs; and identify pathophysiologic condinormal conditions, if 1000 mL of oxygen is avail© Jones
& by
Bartlett
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LLCthat can alter neurologic
© function.
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tions
mon- Learning, LLC
able, 350 mL of oxygen
is used
the body’s
tisNOT
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itoring allows for intraoperative detection OR
of DISTRIBUTION
sues and 650 mL is returned to the lungs; thus the
cerebral ischemia, which may require a change in
normal SVO2 is 65%.
surgical technique to improve or restore perfusion.
Increased MVO2 may be caused by a wedged
It can also be indicated when temporary occlusion
Swan-Ganz catheter (common cause), increased
Jones & Bartlett sepsis,
Learning,
LLC an of a vessel is©planned,
Jonesto&determine
Bartlett the
Learning,
duration LLC
of
FiO2©
, methemoglobinemia,
hypothermia,
NOT cardiac
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tolerance, or
for FOR
titration
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agents
elevated
outputOR
withDISTRIBUTION
left to right shunts,
when pharmacologic metabolic suppression is
neuromuscular paralysis (muscles less active), or
desired.
excessive inotropic drugs.
The impact of anesthetic agents on neurophysiDecreased MVO2 may be caused by a decreased
ologic monitoring
with
the number of
level, a low LLC
oxygen saturation (arterial © Jones
© Jones &hemoglobin
Bartlett Learning,
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Learning,
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synapses
in the OR
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being monitored. This
lowDISTRIBUTION
cardiac output with myocardial dam- NOT
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relationship arises because all anesthetic agents
age, congestive heart failure, hypovolemia, hypoxia,
produce their effects by altering neuronal
orinadequate pulmonary gas exchange. It may also
excitability via changes in synaptic function or
reflect increased tissue demand owing to malignant
axonal
hyperthermia, thyroid
storm, shivering,
fever,
exer© Jones
& Bartlett
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LLC conduction.
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NOT FOR SALE OR DISTRIBUTION
If the MVO2 falls below 30%, the oxygen balance is
ELECTRO ENCEPHALOGRAPHY
compromised and anaerobic metabolism ensues.
EEG has long been regarded as the “gold standard”
for assessing cerebral ischemia during cerebrovas© Jones & Bartlett
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INTRAOPERATIVE
NEUROLOGIC
cular procedures
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as a guide
for toleraNOT FOR SALE
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ble hypotensive
techniques.
The OR
EEG is
a recording
MONITORING
BY THE
of unstimulated brain waves (cortical activity) that
ELECTROPHYSIOLOGIST
results from spontaneous, continuous electrical
1. EEG (electroencephalography):
activity of the brain; it measures electrical activity
• BIS
of the neurons
of the
cerebral cortex.
© Jones & Bartlett
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© Jones
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• PSA 4000
may
be
used
as
a
marker
for
detection
of ischemia
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2. Evoke potentials:
due to inadequate cerebral blood flow (CBF). The
• Somatosensory (SSEP)
character of the EEG waves depends on the level of
• Auditory (BAER)
metabolic activity of the cerebral cortex and level
• Visual (VEP)
wakefulness.
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• Dermatome (trigeminal)
EEG
involves
continuous
intraoperative
moniNOT
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• Motor (MEP)
toring.
The
EEG
technician
reads
the
EEG
monitor
3. Electromyography.
and analyzes the summative numerical value.
4. Wake-up test.
Changes in the EEG are characterized by alterations
in both frequency
and amplitude
as the
cerebral cor© Jones & Bartlett Learning, LLC
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NEUROPHYSIOLOGIC MONITORING
tex
becomes
increasingly
ischemic.
Changes
range
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from subtle changes, such as mild loss of beta/
Electrophysiological measurements are done to
theta activity with a mild increase in delta frequendetect adequate cerebral perfusion and proper
cies, to isoelectric recordings. Summation of all elecneuronal functioning; protect and monitor the
trical activity and conversion into characteristic
functional integrity of “at risk” neural structures;
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Chapter
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waveforms (see Figure 3-1) is of key interest to the
EEG technician:
Mean Arterial Pressure
50 mm Hg: EEG slows
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• Beta waves: presence
of increased
mental
25–40 mm Hg: flat EEG
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stimulation and with eye opening; 12–42 Hz
• Alpha waves: typical of an awake, resting
patient with the eyes closed; 8–12 Hz
• Theta waves: occur during general anesthesia
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and in healthy children while sleeping; 4–8 Hz
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• Delta waves: occur in deep sleep, general anesthesia, and organic brain disease; less than 4 Hz
20 mm Hg: irreversible damage in normothermic
patient
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Other Uses
of FOR
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NOT
EEG can be used intraoperatively as a means by
which to detect abnormal activity such as spike and
wave interictal events and epileptiform discharge.
EEG is now used for the detection of depth of
These
of recording
are commonly
performed
anesthesia
(via BIS) technology.
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before
and
after
resection
of
epileptic
foci
or temNOT FOR SALE OR DISTRIBUTION
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poral lobectomy. Don’t use propofol in these cases,
Cerebral Blood Flow
as this agent raises the seizure threshold.
Normal CBF is 50 mL/100 g/min.
EEG monitoring is especially useful to evaluate
cerebral
perfusion with clamping of major vessels.
CBF 20 mL/100
g/min:&normal
amplitude
and LLC
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Is also used as a guide with use of hypotensive surlatency components
of
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evoked
potenNOT FOR SALE OR DISTRIBUTION
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gical techniques.
tials are maintained.
CBF 18 mL/100 g/min: has been associated
with significant alterations in EEG signaling.
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of approximately 16 mL/100 g/min; waveforms
are completely abolished at levels below
12 mL/100 g/min.
EEG Burst Suppression
Monitored
an EEG,
burst suppres© by
Jones
& drug-induced
Bartlett Learning,
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sion is aNOT
reversible
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neuronal
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metabolic function (CMRO2 ). It is used as a cerebral protection technique. Burst suppression pattern also occurs with ischemic encephalopathy.
CBF 6 mL/100 g/min: irreversible changes in
characteristic signal of EEG burst suppres© Jones & Bartlett
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EEG signaling.
sion is often recognized with deepening of anesNOT FOR SALE OR DISTRIBUTION
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thesia. This pattern consists of high voltage
BAND
periods of bursts and low voltage periods of supAwake
pression, each lasting from 1.5 to 6 seconds. During
Beta
Mental
12–42 Hz
suppression, low-voltage mixed frequency activity
concentration© Jones & Bartlett Learning, LLC
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can be seen. EEG findings during the suppression
Relaxed
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Alpha
phase are not isoelectric.
Light
8–12 Hz
sedation
EEG burst suppression may be seen with any
anesthetic
when combined with hypothermic
Theta
General
4–8 Hz
anesthesia
technique.
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Delta
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Figure 3-1
EEG Waves, Bands
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• General
anesthetics:
Potent
gases
NOT
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(isoflurane, sevoflurane, enflurane, desflurane)
follow the basic anesthesia-related EEG pattern.
Burst suppression occurs at approximately
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Evoked
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39
1.5 MAC for isoflurane, desflurane, and
anesthesia specialists to assess the level of hypnosevoflurane. Enflurane shows burst suppressis and possible awareness. This technique does
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sion at 2–3 MAC.©Sevoflurane
enflurane
measure anesthetic depth.
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bursts can turn into epileptic seizure activity.
Measurements are calculated
over
15–30SALE
seconds.
• Barbiturates and propofol: These drugs follow
A time delay may occur in rapidly changing states.
a pattern of initial EEG activation followed by
Electrode placement is provided via a prepackdose-related depression. Eventually high doses
aged electrode setup, which is applied to the
© Jones
& Bartlett
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LLC
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Bartlett
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lead
to lengthening
periods
of suppression
patient’s forehead
at the&temple.
TheLearning,
machine sets
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ORofDISTRIBUTION
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alternating
periods
activity (burst supitself up automatically
and
tests conduction.
pression). Pentothal burst suppression doses
Advantages of BIS
are in the range of 10–30 mg/kg total dose.
• Reduced risk of awareness
Barbiturates reduce EEG electrical activity (in
• Better
of responses
a dose-dependent
manner)
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stimulation
Ischemic
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•
Faster wake-up
slowing of EEG activity, with electrical activity
• More cost-effective use of drugs
potentially ceasing altogether depending on
the severity of the event. Cerebral blood flow
BIS readings are affected by electrocautery, pacer
below 18 mL/100©g/min
has&
been
associated
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with significant alterations
in
EEG
signaling.
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BIS Data Interpretation
• Hypothermia: Complete EEG suppression
100: awake
occurs at 15–18°C. Additive effects are noted
with other suppressive factors (e.g., inhaled
70: light hypnotic effects
gases,
barbiturates,
ischemia).
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60: moderate hypnotic effects
• NOT
Hyperventilation:
Hyperventilation
can
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activate excitable seizure foci (burst).
40: deep hypnotic effects
• Ventilation/oxygenation: Hypoxemia can
0: EEG suppression
result in evoked potential deterioration.
Under general
anesthesia,
40–60 isLLC
the desired range.
Burst suppression
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EEG can be multifactorial © Jones
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is no guarantee
the patient will have no
origin,
that we utilize many classes of NOT There
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awareness or recall. Research indicates that levels
drugs and other intraoperative factors influence
above 70 have an increased risk of recall.
the EEG.
BIS is not affected by neuromuscular paralysis.
Note that the background EEG activity of
neonates is much less
regular&than
that for
older
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PSA 4000: Patient State Analysis
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PSA 4000 analyzes a four-channel processed EEG
The following medications are not associated
continuously over regions of the brain. This techwith burst suppression: ketamine, benzodiazepines,
nology uses quantitative EEG; it removes artifacts—
opiates, halothane.
both physiologic and environmental—as well.
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BISMonitor:
Bispectral
Analysis
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Bispectral analysis requires fewer electrodes and
gives a global assessment of EEG rather than evaluation of specific areas of the brain. It is used by
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EVOKED POTENTIALS
Evoked potentials (EP), measured from either the
cortex or periphery, are generated in response to
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Chapter
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some stimulus or behavior. This information is
The choice of electrode placement for recording
valuable for monitoring monitor the functional
evoked potentials from the scalp will be dictated
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& Bartlett
Learning, LLC
Jones
Bartlett
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integrity of the ascending
or descending
by the site of stimulation©(see
Figure&3-2).
The critNOT
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(motor) pathways.
ical electrode for detecting the evoked potentialDISTRIBUTION
How sensitive are evoked potentials to
after stimulation of the tibial nerve must be placed
anesthesia?
over the primary sensory cortex at the midline of
the scalp. If the ulnar nerve is stimulated, the elecLeast sensitive:
BAER
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trode must
be placed
over the Learning,
primary sensory
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cortex, somewhat
laterally
from
The integrity of the gracilis and cuneatus tracts
SSEP
of the posterior spinal cord is assessed by SSEP. If
posterior cord or brain ischemia is present, transMost sensitive:
VEP
mission
of actionLearning,
potentials through
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In general, evoked potentials differ in their sencord or
brain OR
will be
diminished, thereby reducing
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sitivity to anesthetic agents depending on the neuthe intensity and delaying the arrival of action
rologic pathways involved and the agent being
potentials in reaching the cerebral cortex.
used. The impact of anesthetic agents on neuroStimulation of a peripheral nerve results in an
physiologic monitoring increases with the number
ascending volley of action©potentials,
travels
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Jones &which
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of synapses in©the
pathway
being monitored.
ipsilaterally
via
the
fasiculus
gracilis
or
cuneatus
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This relationship
arises
all anesthetic
the dorsal columns and first synapses at the dorsal
agents produce their effects by altering neuronal
column nuclei at the cervico-medullary junction.
excitability via changes in synaptic function or
At this point the volley crosses the midline via the
axonal conduction.
medial lemniscal
traverses
the LLC
brain
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& Bartlett
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stem, andNOT
synapses
the thalamus.
From here, the
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Sensory Pathways: Ascending
volley ultimately synapses in the primary
somatosensory cortex or post-central gyrus.
Somatosensory Evoked Potentials
Noninvasive measurement of the brain stem’s
While best known for monitoring during spinal surresponse to repetitive stimulation of a distal sengery, somatosensory evoked potentials (SSEP)
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sory peripheral nerve is possible with SSEP. This
have been used to monitor for ischemia in cortical
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technology assesses the integrity of the sensory
tissue. They are used to determine the adequacy of
pathway in the posterior column of the spinal cord.
collateral blood flow, tolerance of vessel occlusion,
SEEP monitoring measures sensory perception and
and tolerance of hypotensive technique during
does not ensure intact motor response. For SSEP
intracranial surgery. A change in SSEP cortical
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monitoring to be useful,©the
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ischemia.
must exist.
For SSEP monitoring, the stimulating electrodes
The most common peripheral nerves monitored
are placed at a peripheral nerve while the response
are the median (wrist), common peroneal (knee),
is recorded at the contralateral sensory cortex via
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Jones
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or the posterior
(ankle).Learning,
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scalp
electrodes.
Because
the pathway
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measures both latency (how long) and amplitude
goes into the brain from the periphery. Use of multi(how big) of the waveform. A change in SSEP cortiple recording sites allows for coverage along the
cal amplitude is the most sensitive indicator of
entire neural axis, from peripheral stimulus to the
ischemia or some interruption in the posterior
primary somatosensory cortex.
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Evoked
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Primary motor
cortex
(precentral
gyrus)
Frontal
lobe
Primary sensory
cortex
(postcentral
gyrus)
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Parietal lobe
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Temporal lobe
Occipital
lobe
Toes
Trunk
Neck
Head
Shoulder
Arm
Elbow
Fore
arm
Arm
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Litt H rist
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Knee
Foo
t
Toes
Genitals
b
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k
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ey
d and
Eyeli
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Face
Th
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Ey
No
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Fac
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h,
Lips, teet
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gums, an
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41
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(b)
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Figure
3-2 Primary
Motor
(a) and Sensory
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that requiring retraction of the brain stem), during
column pathway. A greater than 50% decrease in
surgery near the primary somatosensory cortex
amplitude or a greater than 10% increase in latency
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BartlettanLearning,
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© Jones
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and during supratentorial surgeries. Moreover, it is
interruption of the posterior spinal
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valuable in assessing lumbar and sacral nerve
Elevated ICP is associated with
roots in posterior interbody fusion, lumbar fusion
reductions in amplitude and increases in latency of
with instrumentation, and cauda equine surgeries;
cortically generated SSEPs; by virtue of its effect on
during carotid endarterectomy, scoliosis repair,
cortical structures, this increase in ICP produces a
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geries; in cervical surgery with instrumentation;
responses.
and in cardiac procedures where cardiopulmonary
SSEP monitoring is used to determine the adebypass is used.
quacy of collateral blood flow, tolerance of vessel
occlusion, and tolerance of hypotensive technique
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and&SSEP
Monitoring
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While it is best
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It is essential to communicate changesDISTRIBUTION
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for its utility during spinal surgery (especially
spinal fusion), this type of monitoring has also
level to neurophysiology staff. It is best to keep anesbeen used to check for ischemia in cortical tissue
thesia at constant levels, especially during critical
during surgery in the posterior fossae (especially
points of surgery. Neurophysiology personnel will
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determine which agents may or may not be used
IV Agents
and what their dose limits are.
• Barbiturates cause dose-dependent reduction
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SSEP monitoring
offers intermediate
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but Learning, LLC
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to anesthetics. In general, an anesthetic technique
waveforms are still present at doses high OR DISTRIBUTION
involving the use of a low-dose inhalational agent
enough to suppress the EEG.
(at “half-MAC”: minimum alveolar concentration.)
• Propofol decreases SSEP amplitude and
along with a narcotic infusion and nitrous oxide at
increases SSEP latency.
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with oxygen
at 33%Learning,
provides the
most stable
• Opioids
cause dose-dependent
decreasedLLC
NOToptimal
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NOTand
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OR DISTRIBUTION
and
conditions
for monitoring nerve
amplitude
increased
High-dose
function.
fentanyl (60 mcg/kg) is still compatible with
SSEP monitoring. Morphine has effects similar
Volatile Anesthetics N2O and inhaled anesthetics
to those of fentanyl. Avoid large boluses at
have the greatest effects to SSEP. Nevertheless, all
of potential
neural
compromise.
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anesthetic agents depress SSEP amplitude in doseMeperidine
canDISTRIBUTION
decrease or increase SSEP
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dependent manner, including nitrous oxide. This
amplitude.
effect varies from isoflurane (most potent) to
• Benzodiazepines also decrease SSEP
enflurane (intermediate potency) to halothane
amplitude. Midazolam has no effect on
( least potent). Sevoflurane and desflurane have
© Jones & Bartlett Learning, LLC latency.
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similar effects to isoflurane when the patient is at
•
Droperidol
has
varying
effects
on SALE
SSEPs but
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a steady state; however, because of their more
can decrease their amplitude.
rapid onset and offset of effect (both are more
• Drugs that can increase amplitude include
insoluble than isoflurane), they may appear to be
etomidate (can be used to enhance SSEPs),
more potent during periods when concentrations
ketamine,
meperidine,
and methohexital.
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areJones
increasing.
•
Muscle
relaxants
have
no
effect
on SSEPs.
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Good
SSEPSALE
monitoring
is compatible with 0.5–1
However, these agent cannot be used if
MAC isoflurane and 60% N2O and oxygen, after
the team is evaluating motor evoked
which the waveforms are lost.
potentials.
SystemicLearning,
Factors
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Brain SALE
Stem Auditory
Evoked Responses
pressure: Mean arterial pressures below
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Brain stem auditory evoked responses ( BAER),
the threshold for cerebral auto regulation via
also known as brain stem auditory evoked potenblood loss or drug effects result in progressive
tials ( BAEP), record data from the scalp that are
decreases in amplitude until loss of the wavegenerated in response ©
to Jones
an auditory
stimulus
form occurs© (but
no &changes
latency). LLC
Jones
BartlettinLearning,
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applied
to
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ear
via
an
external
or
insert
ear-DISTRIBUTION
HypotensionNOT
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“safe”
combined
with
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phone. This placement monitors posterior fossa
surgical manipulation can result in spinal cord
and brain stem activity for cranial nerve VIII (audiischemia.
tory). BAERs are generated in response to depoTemperature: Hyperthermia leads to decreased
larization of the cochlear nerve and are processed
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amplitude
of SSEPs,Learning,
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waves occuralmost entirely in the three divisions of the brain
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ring at 42°C.
stem. Such a potential can arise secondary to compression or ischemia to the nerve or brain stem.
Blood gases/hematocrit: Hypoxia and severe
BAERs are reflected as changes in both amplitude
drops in HCT have been reported to lead to
and latency in high-frequency deflections termed
decreased amplitude of SSEPs.
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Evoked
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Jewett waves. Each wave has a specific site of genevoked potentials (DEP), also known as trigeminal
eration along the auditory axis and can provide
evoked potentials. Stimulation of a single dermatome
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the interpreter with
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about specific
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root Learning, LLC
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sites of pathology.
and subsequent ascending conduction of a signal
via the dorsal column pathways to the primary
BAERs are very resistant to (essentially unafsomatosensory cortex. SSEPs and other evoked
fected by) anesthetics. BAER monitoring is a good
potentials assess a mixed nerve root and do not
choice for surgeries on posterior fossae or in
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& stem
Bartlett
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individualLearning,
nerve roots.
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it is also effective
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Input to theNOT
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for example,
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nerve resection, posterior fossae masses, verteroot levels.
bral-basilar aneurysms, brain stem lesions (meninIn DEP monitoring, electrodes are placed several
gioma), or posterior circulation aneurysms.
centimeters
apart within
a singleLLC
dermatome. The
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keyFOR
problem
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Potentials
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Anatomical pathways
Visual evoked potentials (VEP) are recorded from
and alarm criteria with regard to changes in DEPs
the scalp in response to a visual stimulus provided
are the same as with SSEPs.
in the form of either a flash or a changing checkerDermatome monitoring is©used
during
surgery Learning, LLC
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plexus
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fiber
explorations,
and
spina
bifida/tethered
cord
optic leads or goggles fitted very close to the
releases.
patient’s eyes. A potential is recorded from electrodes placed over the occipital cortex. Changes in
latency,
phase,&and
amplitude
of the VEP
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Motor
Pathways:
Descending
used
to assess
the visual
integrity. The
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primary visual pathway consists of the retina
Motor Evoked Potentials
(receptor), the optic nerves/tracts (pathway), and
Motor evoked potential (MEP) monitoring tests for
the pathway from the thalamus to the primary
the adequacy of perfusion of ventral spinal cord
visual cortex.
and the&motor
pathways.
MEPs monitor
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VEPs are extremely (most) sensitive to anesof FOR
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to the surgical site)
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thetic agents; they are obliterated with inhaled
while recording motor responses (distal to the suragents. VEP monitoring is useful for surgery near
gical site) from the arms and legs. They are recorded
the optic pathway, especially during pituitary
as nerve action potentials from peripheral nerves
surgery; surgery targeting supra- and infra-sellar
from the distal musculature
(compound
muscle Learning, LLC
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tumors; surgery focused on optic nerve tumors
action
potential).
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actiNOT FOR SALE
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and decompression; surgery on occipital cortical
vated, information flows to the ipsilateral thalamus
masses; and pallidotomy, which involves destrucand subsequently to lower motor neurons after
tion of part of the globus pallidus, a region of the
crossing over at the level of the brain stem. These
brain involved with the control of movement.
same pathways can be activated via stimulation of
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Dermatome Evoked Potentials
Sensory evoked potentials can also be useful in evaluating a single segmental (dermatome) nerve root
function; this technique focuses on dermatome
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the brain stem or stimulation of the spinal cord
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directly.
MEP monitoring is used in procedures involving
anterior approaches to the spinal cord, abdominal
aortic aneurysms, scoliosis repair, intradural and
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Chapter
3 Special
Techniques and Concepts
in Anesthesia
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Neuromuscular junction stimulation is essential
for EMG. Thus one cannot use this type of moniLLC
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toring when muscle relaxants
have&
been
adminisNOT
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tered; one can use total intravenous anesthesiaDISTRIBUTION
• MEPs recorded from the musculature are
(TIVA) and inhalation at low doses, however. EMG
abolished easily by halogenated inhalational
monitoring is especially used for facial nerve and
agents.
some spinal surgeries; it can be used in such cases
• Transcranially elicited MEPs are interfered
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Jonesand
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to detect©muscle
nerve disorders.
Profound
with markedly by anesthetics.
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neuromuscular
blockade
will OR
prevent
recording of
• Muscle relaxants cannot be used with MEP
EMG activity during MEP recordings.
monitoring. Muscle relaxation will reduce the
MEP cranial nerve monitoring can be used durability to detect nerve irritation and quantify
ing procedures related to acoustic neuromas,
functional integrity.
microvascular
© Jones & Bartlett Learning, LLC
© Jones
& Bartlettdecompression,
Learning, LLCposterior fossae
• When recordable, MEPs may occur only at low
tumors,
facialOR
nerve
surgery, spinal surgery, skull
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(e.g., 0.2–0.5%).
base procedures, and ENT procedures (tympa• The effect of the inhalational agent is likely the
nomastoidectomy, cochlear implants). It is also
result of depression of synaptic transmission
useful for peripheral nerve explorations, including
either in the anterior horn cell synapses on
brachial plexus explorations,
sciatic
explo© Jones
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Learning,
LLC
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& nerve
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Learning, LLC
motor neurons
or in the&cortex
at the
level of
rations,
and
lumbosacral
explorations
and
fusions
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NOTconnections.
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the interneuronal
(e.g., pedicle screw fusions, tethered cord releases,
• As with the barbiturates, midazolam produces
dorsal rhizotomy, and interbody cage fusions).
a prolonged, marked depression of MEPs.
intramedullary spinal cord tumors, spinal decompression and fusion.
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Anesthesia during
MEP monitoring:
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ELECTROMYOGRAPHY
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WAKE-UP TEST
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Electromyography (EMG) provides real-time inforThe wake-up test is intended to measure the
mation about the integrity of the cranial nerves
patient’s motor function. The surgeon will indicate
and their underlying brain stem nuclei, the muscles
when a patient should be awakened during surgery.
innervated by cranial nerves, and the muscles
The patient will be asked to wiggle his or her toes
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Learning, LLC
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innervated by spinal nerve roots. EMG monitoring
on command upon wakening from anesthesia and
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is especially useful if there is any potential for inadwill then be put back to sleep.
vertent resection of cranial nerves V, VII, IX, and X
Desflurane, which offers a quick wake-up profile,
during brain surgery. It is typically recorded by
is a volatile anesthesia option that is commonly used
placing bipolar pairs of needle electrodes in the
in today’s OR. If nerve paralysis is used, it is allowed
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&
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muscle groups of interest.
to resolve before wake-up
occurs.&Use
of small
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An alarm criterion for EMG recording is simply
amounts of propofol and a narcotic can help keepDISTRIBUTION
the presence of a signal. A baseline or “normal” sitthe patient sleepy (and not coughing and bucking),
uation is the absence of spontaneous muscle activyet still able to follow commands. Dexmedetomidine
ity. Different grades of spontaneous activity results
is also helpful in that patients remain sedated but
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in Jones
different& levels
of alert
(i.e., neurotonic
diseasily awaken
to voice
commands.
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charges or injury potentials). Significant change is
It is important for patients toDISTRIBUTION
have thorough
often unilateral and typically abrupt; it is not
preoperative teaching and explanation to pre necessarily correlative to a particular surgical
pare them for having a “wake-up test.” The patient
maneuver.
should not be in severe pain and will be immediately
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Anesthetics
and Body States ©
Influencing
Neurologic
Monitoring
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45
this medication can produce hallucinations in
some patients.
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© Jones &induction
Bartlett Learning, LLC
Thiopental, a popular barbiturate
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agent, reasults in a transient decrease in amplitude
ANESTHETICS AND BODY STATES
and an increase in latency of cortical responses
INFLUENCING INTRAOPERATIVE
occurring immediately after induction. Minimal
NEUROLOGIC MONITORING
effects are seen on the subcortical and peripheral
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& Bartlettagents
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LLCone of responses. © Jones & Bartlett Learning, LLC
The©effects
of anesthetic
result from
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MEPs areNOT
unusually
to DISTRIBUTION
barbiturates,
twoNOT
mechanisms
of action:
with a prolonged effect being observed when these
• Inhibition of synaptic pathways
agents are used. Methohexital is the exception: It
• Indirect action on pathways by changing the
has been found to increase the amplitudes of cortibalance of inhibitory and excitatory influences
cal SSEPs.
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benzodiazepine,
has desirable
WhileOR
mostDISTRIBUTION
anesthetics depress evoked response NOT Midazolam,
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properties of amnesia. When administered at modamplitude and increase latency, some anesthetic
erate doses, it produces a mild depression of cortiagents (etomidate, methohexital, ketamine) enhance
cal SSEPs. Like the barbiturates, midazolam
both SSEP and MEP amplitudes. This phenomenon
produces
of MEPs. Learning, LLC
is thought to occur ©
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a mechanism
whereby
inhi& Bartlett
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© depression
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Like ketamine, etomidateNOT
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tude of cortical SSEP components and increases
Intravenous induction and sedation agents
the amplitude of MEPs.
interact at a number of different receptors. For
Like thiopental, propofol produces amplitude
example, barbiturates, etomidate, propofol, and
depression
in
SSEPs
with rapid
recovery
benzodiazepines
primarily
act
by
enhancing
the
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after
termination
of
infusion
due
to
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acid
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lism. MEPs have demonstrated a similar depressive
(GABA). Binding and activation of the GABA-a
effect on response amplitude.
receptor results in an increase in chloride conducThe neuromuscular blocking agents act at the
tance and a subsequent hyperpolarization resultacetylcholine receptors found at the neuromuscuing in synaptic inhibition.
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lar junction. Because muscle relaxants exert the
Some intravenous agents work by blocking the
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majority of their action at the neuromuscular juncof glutamate via antagonism of a
tion, they have little effect on electrophysiologic
variety of receptor subtypes: NMDA, kainate, and
recordings such as SSEPs, which are not derived
quisqualate. For example, ketamine appears to
from muscle activity. However, profound neurohave its major action by inhibiting the NMDA
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receptor and subsequently reducing sodium flux
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activity during MEP recordings. Partial neuromusand intracellular calcium levels. Other intravenous
cular blockade has the benefit of reducing a subanesthetic agents activate opioid receptors (mu,
stantial portion of patient movement and facilitates
kappa, and delta).
surgical procedures when muscle relaxation is
Ketamine can enhance cortical SSEP ampli© and
Jones
Bartlett Learning,
© Jonesof&tissues.
Bartlett Learning, LLC
needed for retraction
tude
MEP&amplitude.
Its effects onLLC
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Nitrous oxide reduces SSEP cortical
amplitude
cal and peripheral SSEP responses are minimal.
and increases latency when used alone or when
Although this agent is ideal for cases involving
combined with halogenated inhalational agents
intraoperative monitoring, increases in intracraor opioid agents. When anesthetic agents are
nial pressure are associated with ketamine, and
put back under general anesthesia after checking
motor function.
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Chapter
3 Special
Techniques and Concepts
in Anesthesia
© Jones
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Learning,
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compared at equipotent concentrations, nitrous
Blood Rheology
oxide produces more profound changes in cortiChanges in hematocrit can alter both oxygen© Jones
Bartlett
Learning, LLC
© Jones & Bartlett Learning, LLC
cal SSEPs and MEPs
than &
any
other inhalational
carrying capacity and blood viscosity. Maximum
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agent.
oxygen delivery is thought to occur with a
Opioids depress electro excitability by increasmidrange hematocrit (30–32%). Evoked response
ing inward potassium ion ( K ) current and
changes with hematocrit are consistent within this
depressing outward sodium ion current via a
optimal range.
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G-protein
the receptors
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channels.
effects
opioid analgesics (e.g.,
Ventilation/Oxygenation
alfentanil, fentanyl, remifentanil, sufentanil) on
Hypoxemia can result in evoked potential deterioSSEPs and MEPs are weaker than those associration before other clinical parameters show any
ated with inhalational agents. The opioids prochanges. Alterations in carbon dioxide levels are
duce minimal
changes
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known to affect spinal cord and cortical blood
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although there is some depresNOT FOR SALE
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flow. Remarkable SSEP changes occur when the
sion of amplitude and an increase of latency
CO2 tension is extremely low, suggesting that
in the cortical responses. Spinal application of
excessive vasoconstriction may produce ischemia
morphine or fentanyl for postoperative pain
( 20 mm Hg).
management produces
minimal
changes
in SSEPs LLC
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and MEPs.
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Temperature
SSEP and MEP changes can be observed with
hypothermia. These changes are consistent with
Local factors may produce regional ischemia not
those seen with ischemia and anesthesia, in that
predicted
pressure.
For example,
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they are more significant in the cortically recorded
duringFOR
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responses as opposed to the subcortical potenmay be aggravated by spinal distraction, such that
tials. MEPs exhibit a gradual increase in onset
an acceptable limit of systemic hypotension cannot
latency due to slowed conduction time along the
be determined without monitoring. Regional effects
neural axis. An increase in activation threshold
include peripheral nerve ischemia from positioning,
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latencies
is also seen.
tourniquets, or vascular interruption secondary to
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vasospasm. MEPs and SSEPs are both sensitive to
POSTOPERATIVE VISUAL LOSS
spinal cord events produced by vascular ischemia
No single factor has been identified as a cause of
(carotid cross-clamping) or mechanical comprespostoperative visual loss (POVL), although several
sion. These types of potentials may show differen© Jones & Bartlett Learning, LLC
©observed:
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risk factors are commonly
tial sensitivity to ischemic events.
Blood Flow
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Intracranial Pressure
Elevated ICP is associated with reductions in amplitude and increases in latency of SSEPs, leading to a
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loss of brain stem responses with uncal herniation.
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For MEPs, a gradual increase in the onset latency
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• Eye pressure (small risk)
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causative
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In the prone position the risk of POVL
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Tourniquet
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more than 5 hours and if in a prolonged
vascular resistance (PVR) initially result in right venhead down (Trendelenburg) position
tricular hypertrophy (RVH) but will eventually lead
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cranium.
pressures that exceed 30/10 mm Hg. Pulmonary
■
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With administration of increased amounts
vascular bed, pulmonary vasoconstriction, chronic
of IV fluids
■
hypoxia, collagen vascular disease, sickle cell disWith increased intra-abdominal pressure
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ease, congenital
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high altitude,NOT
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orOR
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• Increased
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blood
levels: affects
neurons
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Treatment
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• Identify
and treatLearning,
the underlying
cause.
blood flow
to the eye.
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• Reduce vascular tone.
Repeat
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• Optimize right ventricular function.
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Anesthesia Management if the Patient Has
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have a decreased FRC. A decreased FRC
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subjects the patient to rapid oxygen
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desaturation and hypoxemia.
carefully.
of colloid
is an alternative
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JonesInfusion
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• Inspired oxygen
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to
infusion
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to maintain
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Avoid hemodilution.
the risk of O2 toxicity.
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• Avoid barotrauma with mechanical ventilation;
the heart.
ventilation should be maintained with
• Avoid abdominal compression.
decreased
tidal volumes
and increased
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Keep blood glucose within “tight control”:
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serum blood glucose 80–120 mg/dL.
• Pad the eyes
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TOURNIQUET ISSUES
of 1 mL/kg/h or more.
The
primary objective of tourniquet
use&inBartlett
surgical Learning, LLC
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• Conduct surgery©inJones
the minimal
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time when the patient
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field; this is achieved by applying circumferential
• Maintain an adequate mean arterial blood
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pressure; maintain adequate perfusion
certain situations, tourniquets may be useful for
pressure to the optic nerve.
preventing the undesirable escape of vascular
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PULMONARY HYPERTENSION
ics to an extremity. Orthopedics and plastic
Normal pulmonary circulation is a high-flow, lowsurgery are two specialties that frequently utilize
pressure circuit. Progressive increases in pulmonary
pneumatic tourniquets.
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Chapter
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in Anesthesia
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Prior to Tourniquet Inflation
• Pale coloring is indicative of adequate
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Check to make sure the antibiotic has been given
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Jones of
&inadequate
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•
Extensive mottling is ©
indicative
before the Esmarch bandage and the tourniquet
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exsanguination.
are applied. An adhesive occlusive dressing should
be applied over any open skin before padding and
Tourniquet Pain
the tourniquet are applied. Wrapping the skin (e.g.,
After inflation of the pneumatic tourniquet for 30–60
with cuff padding, cast padding, or soft cotton
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minutes, patients
may
“tourniquet pain,”
wrap) to protect it from the tourniquet itself helps
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accompanied by an increase in heart rate and
to prevent damage to the skin and subcutaneous
blood pressure. Pain should be assessed and mantissue.
aged. A sympathetic response can occur even when
Multiple sizes of tourniquets should be availthe patient is under general anesthesia. Tourniquet
able to ensure an adequate size to encircle the
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LLC in the cuff—minimum
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pain&frequency
withLLC
intensity depending
limb with
enough overlap
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on the type of anesthesia administered: IV regional
3 inches and maximum 6 inches. The overlap itself
epidural spinal general anesthesia.
should lie on the outside of the extremity to avoid
Treatment of tourniquet pain includes regional
nerve sheath compression. Palpate the patient’s
analgesics, opioids, hypnotics for a patient under
distal extremity pulses before inflation to assess
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local anesthesia, and change
in sedation
technique.
baseline pulses.© Jones & Bartlett Learning, LLC
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Local hypothermia appears
to FOR
be a safe
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effec-DISTRIBUTION
The cuff should
be FOR
positioned
largest
tive method of decreasing the adverse effects of
amount of soft tissue. The cuff should not apply
tourniquet ischemia and allowing continuous
pressure to the bend of the elbow or of the knee
tourniquet inflation time to extend safely beyond
when inflated.
the customary
2-hour
Elevate the
operativeLearning,
extremity to
drain blood
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While NOT
the tourniquet
is inflated,
be mindful of
passively,
and
then wrap
extremity tightly with an
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how much narcotic is administered for tourniquet
Esmarch bandage (or equivalent).
pain. As soon as the tourniquet is deflated, this
noxious stimulus will be removed and presence of
Tourniquet Inflation
excessive narcotic may affect the return of spontaIt is the surgeon’s
responsibility
to dictate the tourni
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neous ventilation for patients under general
quetOR
pressure
setting. The setting is based on the
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anesthesia.
patient’s systolic blood pressure, age, and limb
size. Usually, the inflation setting is 50–100 mm Hg
Tourniquet Time: Safe Duration
greater than the patient’s systolic pressure. The
Tourniquets may be applied
for a&maximum
of
inflation pressure
usually 300
mm Hg LLC
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Jones &isBartlett
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2 hours. Tourniquets have
beenFOR
used up
to 4 hours
in the upper extremity
and 400
mm Hg
in DISTRIBUTION
the lower
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with intermittent deflation of the cuff. The miniextremity.
mum time of application should be 20 minutes to
Over-pressurization may cause pain at the tourniprevent release of the local anesthetic into the
quet cuff site; muscle weakness; compression
general circulation.
injuries
to blood
vessels,
nerve, muscle,
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Damage
from
tourniquet
useDISTRIBUTION
can affect the
extremity
paralysis.
Under-pressurization
may
result
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extremity vessels, nerves, or muscle. Direct cuff
in blood in the surgical field, passive congestion of
pressure can cause ischemia with muscle dysfuncthe limb, shock, and hemorrhagic infiltration of a
tion. Any damage to vessels, nerves, and skeletal
nerve.
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Tourniquet
Issues
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49
muscle is usually reversible for tourniquet inflations
of 1–2 hours.
released acid metabolites enter the circulation
upon deflation of the tourniquet cuff, causing tran© Jones & Bartlett Learning,sient
LLCincreases in end-tidal ©
Jones
& Bartlett
carbon
dioxide,
meta- Learning, LLC
Deflation of the Tourniquet
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bolic acidosis, and a decrease in oxygen saturation.
When the tourniquet is deflated, a decrease in blood
The time for clearance of the metabolites depends
pressure occurs as blood is shunted to the extremon the patient’s physiologic status, the extremity
ity. Products of anaerobic metabolism and newly
involved, and the duration of tourniquet inflation.
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