Case Presentation Axillobifemoral Bypass

Christopher M. Baylis, SRNA
Oregon Health and Science University
I have no financial relationship
with the manufacturer of a
commercial product or
provider of a commercial
service that may be discussed
in this presentation.
December 2012 - February 2013
Case Report
80 y/o, ASA 4, Female
Procedure: Axillobifemoral Bypass
Aug 2011 Acute Inf. Wall MI
ECHO: EF- 15%, A.I. w/ mild stenosis, LVH
ECG: SR, old inf. Infarct
Previous CABG (LIMA
METS 3-4, denies SOB w/ exertion
Carotid stenosis (50% bi-lat.)
– LUE fatigue/ ischemia?
– Claudication
Quit Smoking 2009
– 1 ½ PPD x 40+ yrs
Case Report
Pre-op Physical Exam
Wt: 66kg
Ht: 62”
BP: 88/42
HR: 67 (S1 S2)
RR: 10 (CTA Bi-lat)
SpO2: 100%
Temp: 99.3
Upper and lower dentures
Scott Rigdon, CRNA
President of Oregon Association of Nurse
Definition: Axillobifemoral Bypass
Method of surgical revascularization for
the treatment symptomatic aortoiliac
occlusive disease for patients without an
endovascular option or who cannot
undergo an aortofemoral reconstruction.
Axillobifemoral Bypass,
Medical Tunneler
“What is your anesthetic
• This must have been
scheduled in error, we
are out in the sticks!
• Do we have resources
for this?
• Oh please let’s cancel
• Transfer the patient to
the VA where they are
comfortable dealing with
this type of pt. population
General Anesthetic
Regional/ Neuraxial
Combination of above
Isobaric spinal
– Anesthetize groin to mid thorax
Tumescent (administered by
– Anesthetize cephalic portions of the
MAC (Dexmedetomidine gtt)
– Sedation for comfort during the
Isobaric Spinal Anesthesia
CSF Review
Adults: ~500ml CSF/
day predominately from
choroid plexus
– Reabsorbed mostly by
arachnoid granulations
along sagital sinus
– Sagital sinus regulates
CSF pressure 5-15
mmHg (Naglehout)
CSF Review
~140ml CSF present in the subarachnoid
spaces, central canal of cord and
ventricles of the cord and brain.
• 30-80 ml present in spinal canal
– variable amongst patients
CSF Density
Specific Gravity (ratio):
– Density of substance: Density of water
S.G. of CSF=1.004 to 1.008
– Vary r/t temperature, location of fluid in
subarachnoid space (i.e. S.G. lumbar >
ventricles) dependent on proteins present
• S.G. 0.001 per ea. degree change in Celsius
– S.G. increases w/ age
• r/t glucose, protein present in CSF
Resting position of two fluids w/ differing S.G. when
the fluids are mixed (i.e. CSF & LA)
Isobaric = (S.G. CSF to LA = ~ 1.004 to 1.008)
– Stay in approx same location as injected
– Baracity= 1.004 to 1.008
Hyperbaric = (S.G. of L.A. > CSF)
– Sink to lowest anatomical position (gravity & positioning)
– Baracity > 1.008
Hypobaric = (S.G. of L.A. < CSF)
– Float to highest anatomical position
– Baracity <1.004
Glass Spine Model
Clinically change baracity
Hypobaric: dissolving drug in sterile water
Hyperbaric: dissolving drug in 5-8% dextrose
• 0.75% Spinal Bupivicaine
Isobaric: dissolving drug in CSF or NS
• 0.25%-0.5% Isobaric Bupivicaine
• Tetracaine is really the only LA we would
Cardiovascular Effects
• Sympathectomy & venous pooling 
• T1-T4 cardiac accelerators
• Preventative Management:
– Co-loading not pre-load
• Only 28% of LR remains in the intravascular space
at 30min and 20% at 1hr IVC  ISFC (Chestnut)
– α-adrenergic vasoconstrictors
– Sympathomimetic drugs
Respiratory Effects
• Most studies show minimal effects on Vt, RR,
min vent and art blood gas tension w/ midthoracic level
• Phrenic N. rarely paralyzed (C-3,4,5)
– Respiratory arrest occurs r/t inadequate perfusion
to the medulla
• Accessory ABD and intercostals muscles for
vent are impaired = inability to cough and
clear secretions = aspiration risk
• Care to be taken w/ pts that have poor
ventilatory ability
My Choice
Isobaric spinal
– 0.5% spinal Bupivicaine (15mg) w/ 20mcg fentanyl @
– Achieved a T-8 sensory block
• ~ T-6 sympathetic block & T-10 motor block
– Rational:
• minimize sympathectomy
• prevent respiratory compromise (COPD)
Other option was Lumbar epidural
– Gradual sympathectomy
– Post-op pain management
– Not desired by surgeon r/t infection risk, minimal postop pain, rumored to have had a prior bad outcome
Tumescent Anesthesia
Tumescent Anesthesia
Infiltration of large volumes dilute LA
Often used in liposuction for its “wetting
effect” facilitates fat suctioning, local
anesthetic property and decreases blood
loss w/ addition of epinephrine
• 0.05%-0.1% (0.5-1mg/ml) Lidocaine w/ 0.5
to 1.5 mg/L epinephrine
– 500-1000mg Lidocaine/ Liter
• Addition of sodium bicarbonate may
increase absorption, speed of onset and
decrease the pain of infiltration
• Steroids (Trimcinolone) can be added to
decrease scarring and aid healing
Tumescent: Complications
• Even though theses are dilute solutions,
large amounts of LA may be absorbed
leading to toxicity.
– Only used minimal amounts for this procedure
– Epinephrine slows absorption.
Dexmedetomidine (Precedx)
Dexmedetomidine- Overview
• Presynaptic alpha 2- adrenergic agonist
– Sedation & analgesia w/o resp. depression
– Not an amnestic
– Not GABA-mimetic like propofol or
• Approved by FDA in 1999 for use in ICU
• Approved in 2008 for patients requiring
sedation prior to and or during surgical
Dexmedetomidine in the OR
• Current uses:
Awake fiberoptic intubation
Carotid endarterectomies
Procedural sedation
Bariatric surgery
ICU sedation.
Current studies for its place in OB
• Rx preeclamptic patients w/ contraindication to regional anesthesia
• Possible increases uterine contractions = aid labor/ prevent uterine atony
• Used alone or as co-adjunct to decrease amount of volatile agent
and opioids.
• Has been used in epidurals (0.5-1 mcg/kg) to improve duration
and analgesia.
Distribution ½ life= 6minutes
Elimination ½ life = 2 hours
94% protein bound
Almost complete biotransformation in the
liver with urinary excretion of 95%
– Lower doses required with patients with
hepatic or renal disease
Review: Presynaptic Alpha 2
• Alpha-2 receptors are
located presynaptically
in sympathetic nerve
endings and in
noradrenergic neurons
in the CNS.
• Stimulation of these
receptors creates a
negative feedback loop
and decreases the
release of
What other drug that has been
around for a while, works on
the pre-synaptic α2adrenergic receptor?
Alpha 2 Agonist & Sedation
The receptors in the
locus coeruleus of the
upper brain stem and
the substantia
gelatinosa mediate
the sedative effects.
Alpha 2 Agonists & Analgesia
Pain is mediated in
the spinal cord by
alpha 2 receptors
inhibiting transmission
from nociceptive
neurons to relay
neurons in the dorsal
Pros of Dexmedetomidine
• Sedation and analgesia without respiratory
• Easily arousable and responsive to stimulation
without becoming uncomfortable and quick return
to sleep-like state- COOPERATIVE PATIENT
– Patients receiving Precedex have been observed to
be arousable and alert when stimulated. This alone
should not be considered as evidence of lack of
efficacy in the absence of other clinical signs and
• Reduced anesthetic/ analgesic requirements
• Wide margin of safety
Side Effects
• Hypotension, bradycardia and sinus arrest
• Atropine and glycopyrolate were effective
in treating bradycardia in clinical trails
• Should not be administered to those with
heart conduction block, hypotension,
hypovolemia or shock
• Transient HTN seen with loading dose
What to expect
Dexmedetomidine Dosing
• Adults:
– Loading dose of 1 mcg/kg over 10 min- titrate to effect of
sedation desired
– Maintenance infusion 0.2-0.7 mcg/kg/min- titrate to desired
effect of sedation
– If HoTN occurs, decrease/ stop infusion, give fluids, treat
w/ vasopressors
• Lower doses required w/ hepatic or renal disease
• Not indicated for infusion >24hrs
– Has not been tested for greater than this time period
• Dilute prior to administration:
– W/D 2ml of precedex add 48ml of 0.9% NaCl for total of
50ml w/ final concentration of 4mcg/ml
AFOI Protocol
MAC Protocol
Thank You!!!
Jaffe RA, Samuels SI, Schmiesing CA, Golianu B eds. Anesthesiologist’s Manual of
Surgical Procedures. 4th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams
& Wilkins; 2009.
Barash PG, Cullen BF, Stoelting RK, Cahalan M. Clinical Anesthesia. Lippincott
Williams & Wilkins; 2009.
Barash P. Handbook of clinical anesthesia. 6th ed. Philadelphia: Lippincott Williams &
Wilkins; 2009.
Nagelhout JJ, Plaus KL. Handbook of Nurse Anesthesia. Elsevier Health Sciences;
Morgan GE, Mikhail MS, Murray MJ. Clinical anesthesiology. Lange Medical
Books/McGraw Hill; 2005.
Miller, Ronald D, Manuel Pardo, and Robert K. Stoelting. Basics of Anesthesia.
Philadelphia, PA: Elsevier/Saunders, 2011.
Fauci AS, Braunwald E, Kasper DL, et al. Harrison’s Principles of Internal MedicineHarrison’s Online. McGraw-Hill Medical; 2008
Mills, Stacey E., ed. Sternberg’s diagnostic surgical pathology, 4th ed., Philadelphia:
Lippincott Williams & Wilkins, 2004. 2 vol.
Stoelting's Anesthesia and Co-existing Disease, 5th ed. R. L. Hines, and K. E.
Marschall. Saunders Elsevier, Oxford, 2008.
Pandharipande PP, Pun BT, Herr DL, et al. Effect of sedation with dexmedetomidine
vs lorazepam on acute brain dysfunction in mechanically ventilated patients: the
MENDS randomized controlled trial. JAMA. 2007;298(22):2644-2653.
• Dr. John J. Nagelhout
– “>23 factors thought to effect spread of LA in
CSF, therefore affecting level and quality of
– “Clinically the most important are the ones
that can be manipulated by the provider.”
1. Total dose of LA
2. Site of injection
3. Baracity of drug
• Based primarily on L.A. used and total dose
– Highly protein bound drugs (i.e. bupiv, ropiv,
tetracaine) long durations of action
– Less protein bound drugs (i.e. lidocaine, mepivicaine)
shorter duration of action
• Ephedrine: vasoconstriction delays normal uptake
= prolong duration of L.A.
– Greatest w/ Tetricaine, less w/ Lido, minimal w/ Bupiv
• Opioids: synergistic effect w/ L.A. and opioids
• α2-agonist is not clear but result in prolonged L.A.
Anesthetic Record

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