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N934 Advanced Principles of Anesthesia II > Vascular Anesthesia > Flashcards

Vascular Anesthesia Flashcards

1
Q

coexisting diseases

A
  • DM
  • HTN
  • renal impairment
  • pulmonary disease
  • systemic atherosclerosis
  • coronary artery disease
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2
Q

coronary artery disease (CAD)

A
  • leading cause of perioperative mortality at the time of vascular surgery
  • less than 10% of vascular patients who undergo surgery have normal coronaries
  • unrecognized silent MIs occur in 23-28% of patients
  • long term the prevalance of MI and death is 8.9 and 11.2% in patients undergoing vascular surgery
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3
Q

pathology of atherosclerosis

A
  • generalized, progressive, chronic inflammatory disorder of the arterial tree with development of fibrous intimal plaque associated with endothelial dysfunction
  • potentially compromises blood flow to all the organs and extremities leads to MI, stroke, gangrene
  • combo of lipid disorder and inflammatory process
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4
Q

stage I of atherosclerosis

A
  • fatty streak
  • endothelium damaged –> chronic inflammatory response and hypercoagulable state
  • lipoproteins enter intimal layer
  • can start in childhood
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5
Q

stage II of atherosclerosis

A
  • fibrous plaque
  • made of oxidized lipids, inflammatory cells, calcium deposits, etc.
  • blood flow reduction occurs here
  • ischemia to vital organs and extremities
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6
Q

stage III of atherosclerosis

A
  • advanced lesion
  • plaque with necrotic core, calcium accumulation, and endothelial dysfunction
  • physical disruption of plaques protective cap exposes blood to highly thrombogenic material which promotes acute thrombus formation and vasospasm
  • complete occlusion possible at this level
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7
Q

three types of atherosclerotic morbidity

A
  • enlarged plaque reduces lumen of blood vessel (limb ischemia, stable angina)
  • plaque rupture/ulceration, embolization, and thrombus formation
  • atrophy of media with arterial wall weakening (aneurysm dilation)
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8
Q

most common sites for atherosclerotic lesions

A
  • aortoiliac peripheral
  • coronary
  • aortic arch branches
  • combined
  • mesenteric renal
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9
Q

CAD ACC and AHA pre-op evaluation guidelines

A
  • focus = evaluation of patient at risk for CV M&M undergoing non-cardiac surgery
  • goal = best possible quality of care and outcome for the patient
  • goal = information obtained should be used for both peri-op period and to inform the long term treatment plan
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10
Q

components of pre-op guidelines for vascular patients

A
  • clinical history - clinical risk factors, exercise tolerance
  • supplemental evaluation
  • perioperative therapy
  • surgical procedure - low, intermediate or high risk
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11
Q

aspirin

A
  • inhibits platelets

- potential for increased bleeding and decreased GFR

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12
Q

plavix

A
  • inhibits plts

- potential for increased bleeding

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13
Q

statins

A

-can effect liver function

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14
Q

ACE inhibitors

A
  • induction hypotension

- coughing

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15
Q

Diuretics

A
  • hypovolemia

- electrolyte imbalance

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16
Q

ca+ channel blockers

A

-hypotension

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17
Q

hypoglycemic drugs

A
  • hypoglycemia

- lactic acidosis with metformin

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18
Q

beta blockers

A
  • bronchospasm
  • decreased BP
  • decreased HR
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19
Q

other medical management for CAD

A
  • smoking cessation
  • weight loss
  • exercise
  • all the meds
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20
Q

bare metal stent minimum DAPT

A

1-3 months

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21
Q

drug eluting stent minimum DAPT

A
  • 6 months

- so cant do some types of surgery for 6 months post coronary stenting if you have drug eluting stent

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22
Q

causes of periop MIs

A
  • culprit lesions - vulnerable plaques with high likelihood of thrombotic complications; often located in coronary vessels without critical stenosis
  • demand ischemia - predominant cause of periop MI
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23
Q

preop assessment of cardiac function

A
  • advanced cardiac testing used to determine if coronary intervention is needed prior to vascular surgery OR to determine if aggressive intraop and post op management
  • exercise/pharm stress test
  • ECHO
  • assessment of myocardial ischemia, MI, valve dysfunction, heart failure
  • duplex imaging of carotid arteries or angiography
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24
Q

preop assessment of pulmonary function

A
  • the most important pulmonary complications are atelectasis, pneumonia, resp failure, and exacerbation of underlying chronic disease
  • high prevalence of cigarette smoking in this population and COPD common
  • tests - PFTs, ABGs, CXRs
  • consider - incentive spirometry, steroids, regional, abx, and cpap
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25
Q

preop assessment of renal function

A
  • chronic renal disease strongly predicts long term mortality in patients with symptomatic lower extremity arterial occlusive disease
  • tests - serum cr, cr clearance
  • consider - contrast dye use, beta-blockers, statins, volume status, perfusion pressures
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26
Q

lower extremity peripheral artery disease

A

defined as insufficiency in lower extremities presenting with acute or chronic limb ischemia with occlusions distal to the inguinal ligament

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27
Q

lower extremity revascularization

A
  • PAD or atheroslcerotic occlusive disease of lower extremities
  • risk for amputation, MI, stroke, death
  • probable atherosclerosis in other beds
  • DM at extra high risk
  • often on antiplt and anticoags, makes challenging in preop perioid
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28
Q

indications for peripheral revascularization

A
  • acute ischemia due to emboli, thrombus or pseudoaneurysm
  • irreversible ischemic damage occurs 4-6 hours (urgent thrombolytic therapy, arteriography, surgical intervention
  • chronic ischemia due to - athersclerotic plaque progressively narrowing vessel, claudication with eventual thrombosis of vessel
  • surgery indicated when severe disabling claudication, critical limb ischemia
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29
Q

peripheral occlusions traditional surgical approach

A
  • unobstructed blood flow source (donor) artery exposed (usually common femoral, superficial femoral, or deep femoral)
  • target distal artery (recipient) exposed at or below the knee (usually dorsalis pedis or posterior tibial)
  • after donor and recipient arteries exposed, a tunnel is created and graft is passed
  • graft may be saphenous vein or prosthesis
  • IV heparin given
  • anastomosis are constructed
  • arteriogram to confirm adequate flow
  • heparin in not likely to be reversed
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30
Q

what if saphenous vein is used?

A

-if saphenous vein used, the vein is dissected all branches are ligated, divided and excised; saphenous vein is reversed to permit blood flow in direction of valves

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31
Q

anesthetic management for peripheral revascularization

A
  • preop beta blockers and or other chronic med
  • intraop - arterial line
  • continuous EKG monitoring + ST analysis (leads II and V)
  • monitor intravascular volume by foley (+/- CVP or PA cath)
  • minimal blood loss and 3rd space
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32
Q

what do you need for emergency revascularization surgery

A
  • carefully watch K+ levels
  • myoglobinemia
  • fasciotomy may be required
  • coag studies
  • ECG ischemia
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33
Q

regional vs general for peripheral revascularization

A
  • assess for coagulopathy or anticoagulation therapy
  • spinal may be best to avoid hematoma
  • most studies have shown no difference between RA and GA in terms of cardiopulmonary complications
  • significant difference 5x in complication rate in terms of graft occlusion with regional being superior
  • studies regarding efficacy of post op pain management with epidural vs opioids are poorly designed
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34
Q

why is graft occlusion significant with GA in postop period?

A
  • hypercoagulable state with GA as opposed to RA
  • fibrinolysis decreased after GA, therefore fibrinogen not broken down and clots form
  • epi, norepi, and cortisol release increased after GA compared to RA
  • patency of graft maintained with RA secondary to increased blood flow with sympathectomy
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35
Q

what is the appropriate regional anesthesia for peripheral reperfusion

A
  • L1-L4 dermatomes
  • T10 level usually adequate
  • epidural dosing usually 9-12 mL including test dose
  • ELDERLY require decreased dosing
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36
Q

post op management for peripheral revascularization

A
  • control pain and anxiety (high risk for MI in this period)
  • avoid anemia (need Hgb greater than 9-10)
  • control HR and BP
  • frequent checks of peripheral pulses
  • continuous EKG monitoring and ST analysis
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37
Q

lower extremity endovascular treatment anesthetic management

A
  • GA, neuraxial, MAC
  • percutaneous procedures so often MAC
  • open access needed, consider GA instead
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38
Q

what is the principal cause of carotid artery disease?

A

atherosclerosis

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39
Q

where do carotid plaques commonly occur

A
  • common carotid artery

- internal and external carotid arteries

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40
Q

S/S of carotid artery disease

A
  • fatal or debilitating stroke
  • TIA
  • amaurosis fugax (transient attack of mononuclear blindness)
  • asymptomatic bruit
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41
Q

strokes

A
  • 5th leading cause of death in US
  • varies by race/ethnicity
  • 795,000 new strokes each year in US
  • risk factors = HTN, smoking, obesity, DM
  • 87% are ischemic
  • extracranial atherosclerotic disease accounts for up to 20% of all ischemic strokes
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42
Q

Carotid endarterectomy (CEA)

A
  • has been around for 50 years
  • most common peripheral vascular surgical procedure performed in US
  • 130,000 performed annually in US
  • definitive results for symptomatic patients with high-grade carotid stenosis (70-99%)
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43
Q

preop assessment for CEA

A
  • recent symptoms - surgical intervention timing
  • optimize medical management - beta blockers, statins, antiplt therapy, HTN control, restore intravascular volume, reset cerebral autoregulation, DM control
  • CAD is common
  • bad signs = UA, decompensated CHF, significant valve disease
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44
Q

anesthesia for CEA

A
  • awake vs GA/ETT
  • continue ASA throughout periop period
  • continue cardiac meds
  • EKG monitoring should include continuous leads II and V for detection of rhythm disturbances and ST changes
  • a line
  • PIV x2, large bore, arms tucked
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45
Q

lead II measures what?

A

inferior

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46
Q

lead V5 measures what?

A

lateral

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47
Q

CEA case setup

A
  • type and screen
  • a line
  • ACT machine, fluid warmer, lower body bair hugger
  • phenyl and remi in line
  • clevidipine and NTG available
  • beta blockers and ephedrine available
  • heparin and protamine
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48
Q

CEA case monitoring

A
  • routine with V5 lead and ST segment analysis plus a line
  • consider cerebral oximetry
  • occasionally surgeons want to measure stump pressures (so need extra pressure line tubing and blue male to male adapter to connect to a line transducer)
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49
Q

CEA and GA

A
  • sedative pre med
  • fentanyl for awake aline placement
  • induction - prop, etomidate, roc
  • consider esmolol during DL
  • immediate treatment of hyper of hypo tension
  • inhalation agent
  • cerebral oximetry
  • adjuncts - prop, remi, precedex
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50
Q

arterial blood pressure monitoring during CEA

A
  • abp should be maintained in the high-normal range throughout the procedure particularly during the period of carotid clamping to increase collateral flow and prevent cerebral ischemia
  • induced HTN to approximately 10-20% above baseline
  • careful with increased BP, HR, and myocardial demand
  • MAKE SURE to note preinduction MAP
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51
Q

what happens with surgical manipulation of carotid sinus?

A
  • baroreceptor reflex
  • HR will decreased
  • BP will decrease
  • cessation of surgical stim promptly restores hemodynamics
  • infiltration of carotid bifurcation with 1% lido usually prevents further episodes
52
Q

emergence for CEA

A
  • neuro deficits on emergence require immediate discussion with the surgeon about the need for angiography, reoperation, or both
  • emergence may be associated with marked hypertension and tachy –> need aggressive pharmacologic intervention
53
Q

regional anesthesia for CEA

A
  • blocking C2-C4 dermatomes by use of superficial, intermediate, deep or combined cervical plexus block
  • regional and local anesthesia allow continuous neuro assessment
  • reduces need for shunt
  • greater hemodynamic stability
  • reduced cost
  • requires patient cooperation
  • conversion to GA 2-6%
54
Q

superficial cervical plexus block

A
  • midpoint of posterior border of SCM muscle
  • injection along posterior border of medial surface of the muscle
  • may block accessory nerve causing trapezius muscle paralysis
55
Q

cerebral autoregulation

A
  • hypocapnia - decrease CBF (vasoconstrict)
  • hypercapnia - increase CBF (vasodilate)
  • if there is poor collateralization and resultant cerebral hypoperfusion, cerebral resistance vessels in hypo-perfused territories will dilate to maintain cerebral blood flow
56
Q

carotid artery stump pressure

A
  • internal carotid artery stump pressure represents the back-pressure resulting from collateral flow through the circle of Willis via the contralateral carotid artery and vertebrobasilar system
  • ideally above 45-50 mmHg
  • may or may not be done
57
Q

cerebral NIRS

A
  • non-invasive technique that allows continuous monitoring of regional cerebral oxygen sat through scalp and skull
  • based on absorption characteristics of oxygenated vs deoxygenated blood
  • measure O2 sat of Hgb in entire tissue bed (brain, arterial, and venous)
  • predominantly venous so therefore approximates VENOUS blood O2 sat
58
Q

CEA post op complications

A
  • HTN - surgical denervation of carotid sinus baroreceptors
  • HoTN - baroreceptor hypersensitivity or reactivation
  • cerebral hyper-perfusion syndrome - abrupt increase in blood flow with loss of autoregulation
  • cranial and cervical nerve dysfunction (RLN, SLN, hypoglossal, mandibular)
  • carotid body denervation
  • wound hematoma
59
Q

s/s cerebral hyperperfusion syndrome

A
  • HA
  • seizure
  • focal neurologic signs
  • brain edema
  • intracerebral hemorrhage
60
Q

bilateral RLN dmage

A
  • results in bilateral vocal cord paralysis

- life threatening upper airway obstruction

61
Q

s/s carotid body denervation

A
  • impaired ventilatory response to mild hypoxemia
  • central chemoreceptors impaired
  • worsened with opioid admin
62
Q

aortic aneurysm

A
  • dilation of all 3 layers of an artery
  • occasionally produce symptoms of compression on surrounding areas
  • s/s - may be asymptomatic or present with pain mostly due to compression of adjacent structures or vessels
63
Q

aortic dissection

A
  • surgical emergency
  • mortality up to 58%
  • occurs when blood enters the medial layer
  • initiation occurs with a tear in the intimal layer
  • can occur over minute to hours
  • s/s - severe sharp pain in the posterior chest or back pain
64
Q

three layers of aorta

A
  • intima (inner most)
  • media
  • adventitia (outermost)
65
Q

abdominal aortic aneursym risk factors

A
  • elderly, male
  • smoking
  • family history of AAA
  • athersclerotic disease and HTN
66
Q

contributing factors to adventitial elastin degradation

A
  • genetic
  • biochemical
  • metabolic
  • infectious
  • mechanical
  • hemodynamic
67
Q

AAA

A
  • asymptomatic pulsatile abdominal mass
  • concomitant aortoiliac occlusive disease is present in approximately 20-25% of patients
  • rare causes include trauma, myocotic infection, syphilis, marfan
68
Q

elective AAA repair… WHEN?

A
  • done 6cm or larger
  • controversial if it is 5.5-5.9 cm
  • aneurysms less than 4.0 cm in diameter are thought to be relatively benign in terms of rupture and expansion
  • surgery may be considered for smaller aneurysms if they become symptomatic
69
Q

law of LaPlace

A
  • increasing diameter is associated with increased wall tension, even when arterial pressure is constant
  • the frequent incidence of associated systemic HTN enhances aneurysm enlargent
70
Q

ruptured AAA

A
  • periop mortality for ruptured AAA is around 50%

- death before reaching hospital is >90%

71
Q

classic triad of ruptured AAA

A
  • hypotension
  • back pain
  • pulsatile abdominal mass
72
Q

EVAR technique

A
  • used for all types of aortic diseases (trauma, rupture, dissection)
  • less invasive
  • reduced M&M
  • shorter hospital stay
  • now most common technique for AAA repair
  • femoral arteries are accessed either by cutdown or percutaneous punctures
73
Q

anesthesia for EVAR

A
  • MAC with local/regional vs GA
  • consider patient’s functional status
  • steering guiding sheaths that may require L arm arterial cutdown
  • spinal cord - extensive collateral network
  • hemodynamic management
  • preservation of organ perfusion
  • blood loss and intravascular volume
  • temperature
  • risk of conversion to open
  • radiation safety
74
Q

two most important factors that contribute to CIN

A
  • contrast load

- preexisting kidney disease

75
Q

how to prevent CIN

A
  • limit contrast load

- adequate hydration to decrease viscosity of idodine based dyes

76
Q

EVAR early complications

A
  • paraplegia
  • stroke
  • ARI
  • aneurysm rupture
  • pelvic hematoma
77
Q

EVAR late complications

A
  • endoleaks
  • aneurysm rupture
  • device migration
  • limb occlusion
  • graft infection
78
Q

endoleak

A
  • normally tx with balloon angioplasty of proximal attachment site so that the desired seal is obtained through remodeling of stent-graft
  • type II endoleak - treated with transarterial embolization through iliac arteries or retrograde embolization through superior mesenteric or inferior mesenteric arteries
  • open surgical treatment also an option
79
Q

open abdominal aortic reconstruction

A
  • large incisions and extensive dissection
  • clamping and unclamping of aortic or its major branches
  • varying duration of organ ischemia reperfusion
  • significant fluid shifts
  • temperature fluctuations
  • activation of neurohumoral and inflammatory responses
80
Q

aortoiliac occlusive disease

A
  • infrarenal aorta and iliac arteries are two of the most common sites of chronic atherosclerosis
  • diffuse and progressive plaque enlargement may reduce blood flow to the lower extremities below a critical level and result in symptoms of ischemia
  • patients have surgery only if symptomatic (claducation and ischemia)
81
Q

management of aortoiliac occlusive disease

A
  • direct reconstruction (gold standard)
  • extra-anatomic or indirect bypass graft
  • catheter based endoluminal techniques (for local disease)
82
Q

patho of aortic cross clamping depends on what?

A
  • level of cross clamp
  • status of LV
  • degree of periaortic collateralization
  • intravascular blood volume and distribution
  • activation of SNS
  • anesthetic drugs and techniques
  • heparinization
  • monitor ACTs
83
Q

Aortic cross clamp above the clamp

A

arterial hypertension

84
Q

aortic cross clamp below the clamp

A

arterial hypotension

85
Q

common ischemic complications with aortic cross clamp

A
  • renal failure
  • hepatic ischemia
  • coagulopathy
  • bowel infarction
  • paraplegia
86
Q

thoracic aortic cross clamp effects

A
  • increased MAP
  • increased CVP
  • increased mean pulmonary arterial
  • increased pulmonary wedge
  • decreased cardiac index
  • decreased EF
  • no change in HR
87
Q

aortic cross clamp metabolic effects

A
  • decreases total body O2 consumption by 50%
  • blood flow through tissues and organs below the level of aortic occlusion is DEPENDENT ON PERFUSION PRESSURE and is independent of cardiac output
88
Q

management during aortic cross clamp

A
  • acute increase in SVR and decreased CO
  • the higher the clamp the more significant the impact on perfusion to vital organs
  • use vasodilators to decrease afterload, wall stress, and myocardial oxygen demand
  • avoid long acting meds
  • perfusion to distal organs is dependent on collaterals which originate proximal to the clamp or shunts
89
Q

renal effects of aortic cross clamp

A
  • clamp above renal arteries decrease renal blood flow up to 80-90%
  • epidural anesthesia does not reduce/prevent impairment of renal perfusion
  • preop renal insufficiency is STRONGEST predictor of post op renal dysufnction
90
Q

renal protection during aortic cross clamp

A
  • controversial
  • mannitol (12.5 g/70kg)
  • loop diuretics
  • methylprednisolone
  • dopamine (1-3 mcg/kg/min)
91
Q

mannitol renal protective effects

A
  • improves renal cortical blood flow
  • scavenges free radicals
  • decreases renin secretion
  • increases renal prostaglandin synthesis
92
Q

what cardiac dysfunctions are most vulnerable to stress of aortic cross clamp

A
  • preexisting impaired ventricular function

- reduced coronary reserve

93
Q

goals during cross clamp for those with pre-existing cardiac dysfunction

A
  • reduce afterload (nitroprusside, clevidipine)
  • maintain normal preload (IVF)
  • maintain CO (inotropes, MAP goals)
94
Q

aortic unclamping

A
  • massive hemodynamic response
  • hypotension
  • reactive hyperemia
  • washout of vasoactive and cardio-depressant mediators
  • pulmonary hypervolemia (flash pulm edema picture)
95
Q

how severe the hemodynamic response to unclamping is depends on what?

A
  • level of aortic occlusion
  • total occlusion time
  • use of diverting support
  • intravascular volume
96
Q

therapeutic interventions to unclamping

A
  • decrease inhaled agents
  • decrease vasodilators
  • increase IVF
  • increase vasoconstrictor drugs
  • reapply cross clamp for SEVERE hypotension
  • consider mannitol
  • consider sodium bicarb
97
Q

anesthetic management for open AAA

A
  • rapid blood loss possible - LARGE PIVs, a line, central line, cross-matched blood, cell salvage
  • TEE
  • cerebral oximetry
  • techniques = GA/ETT, regional, combined, low volatile
  • esmolol, nitroprusside, nitroglycerin, clevidpine, phenyl READY TO GO
  • heparin + protamine
  • monitor ACT
  • temperature control - do not warm below the clamp, this could increase ischemic injury by increasing metabolic demand
98
Q

heparin dose

A

100-300 units/kg

99
Q

hemodynamic management for AAA

A
  • HTN avoided bc acute stress on aneurysm can cause rupture
  • HR maintained at or below baseline
  • euvolemic resuscitation may be deferred until aortic rupture surgically controlled in OR
100
Q

post op management for AAA

A
  • tight control of HTN and tachycardia
  • homeostasis of hemodynamics, metabolic, and temp prior to extubation
  • LOS is variable
  • pain - epidural vs PCA
101
Q

complications in post op period for AAA

A
  • MI
  • pneumonia
  • sepsis
  • renal failure
  • decreased tissue perfusion
  • hypothermia
102
Q

thoracic aortic aneurysm

A

-associated with genetic syndromes - marfan, ehlers-danlos, bicuspid aortic valve, non-syndromaic familial aortic dissection

103
Q

repair approach for thoracic aortic aneurysm

A
  • descending aorta - left posterolateral thoracotomy (w OLV)
  • ascending aorta - supine, median sternotomy
  • full or partial CPB
104
Q

S/S thoracic aortic aneurysms

A
  • s/s result of impingement of surrounding structures
  • hoarseness results form stretching of L RLN
  • stridor due to compression of trachea
  • dysphagia due to compression of esophagus
  • dyspnea due to compression of lungs
  • edema from compression of SVC
105
Q

thoracic aortic dissection symptoms

A
  • acute, severe sharp pain in anterior chest, neck, or between shoulder blades
  • dimunition or absence of peripheral pulses
106
Q

Crawford type I for TAA

A

aneurysm involving descending thoracic aorta and upper abdominal aorta

107
Q

Crawford type II for TAA

A

descending thoracic and most abdominal aorta

108
Q

Crawford type III for TAA

A

lower thoracic aorta and most abdominal aorta

109
Q

Crawford type IV for TAA

A

most or all abdominal aorta

110
Q

most difficult crawford TAA types to repair

A

types II and III

111
Q

DeBakey Classification of Dissecting AA Type I

A

ascending aortic tear with dissection down entire aorta

112
Q

DeBakey Classification of Dissecting AA Type II

A

tear in ascending aorta with dissection limited to ascending aorta

113
Q

DeBakey Classification of Dissecting AA Type III

A

tear in proximal descending thoracic aorta with dissection from thoracic aorta to abdominal aorta

114
Q

spinal cord perfusion

A
  • two posterior arteries (25% blood flow)
  • one anterior artery (75% blood flow)
  • largest radicular artery = artery of Adamkiewicz (AKA)
115
Q

artery of adamkiewicz (AKA)

A
  • major blood supply to lower 2/3 of spinal cord
  • segmental supplier of AKA is usually located between T9-T12 75% of the time
  • can be T5-L5 (VARIABLE)
116
Q

anterior spinal artery syndrome

A
  • flaccid paralysis of lower extremities
  • bowel and bladder dysfunction
  • sensation + proprioception are SPARED!!!
117
Q

spinal cord protection

A
  • limit x-clamp time < 30 min
  • distal aortic perfusion (ECMO)
  • CSF drainage - to decrease pressure in spinal cord and increase perfusion)
  • intrathecal papaverine (help increase BF to area)
  • mild hypothermia to reduce O2 requirements
  • barbiturates
  • corticosteroids
  • avoid hyperglycemia
118
Q

SSEPs

A

posterior lateral cord, sensory

119
Q

MEPs

A

anterior cord, motor

120
Q

what is indication of SCI

A

reduction in MEP amplitude to less than 25% of baseline

may require corrective measures

121
Q

what things in anesthesia effect MEPs (i.e. things we cannot use)

A
  • muscle relaxation

- inhaled agents

122
Q

TAA preop prep + monitoring

A
  • know extent of aneurysm TALK TO SURGICAL TEAM
  • PRBCs, FFP, plts
  • invasive lines - aline, PA cath, CSF Pressure, LARGE BORE IV
  • TEE common
  • R fem artery cath to monitor BP distal to clamp
  • Double lumen ETT or bronchial blocker for OLV
  • position = thoracoabdominal incision + retroperitoneal dissection
  • SSEPs + MEPs
  • body temp
123
Q

where do you put the a line in TAA surgery

A

R radial because cross clamp may be placed proximal to L subclavian artery which occludes flow to LUE

124
Q

TAA anesthetic technique

A
  • induction slow and controlled to avoid aneurysm rupture
  • usually a balanced anesthetic
  • opioid, low dose volatile, benzo, NDMR
  • TIVA if MEP
  • consider combined epidural/GA
  • +/- thoracic epidural for post op pain
  • Extubate in ICU
125
Q

TAA post op care

A
  • may consider extubation in OR
  • normally not tho and done in ICU
  • admit to ICU DUH

N934 Advanced Principles of Anesthesia II (17 decks)

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