Vascular PPT Flashcards
Ascending aorta starts at the _ _ and ends at the _ _ (sternal angle ~ _ or _ rib)
aortic valve
aortic arch
2nd or 3rd rib
Aortic arch starts at the _ of the _ aorta and ends _ the origin of the 3 main arteries (brachiocephalic trunk, LCCA, and L subclavian) around _ level.
arch of the ascending aorta
after
TV4
The descending aorta has 2 parts: the thoracic which starts at the _ _ and ends at the _ (~ _ level) and the abdominal aorta which starts from below the _ and goes until the _ of the _ _ arteries (~ _ level).
Thoracic: aortic arch - diaphragm
-TV12
Abdominal: below the diaphragm – bifurcation of common iliac arteries
-LV4
The bifurcation of the aorta is at _ level which then splits into the R + L _ _ arteries
LV4
R+L common iliac
The 5 branches of the abdominal aorta before the bifurcation incluse:
celiac trunk
Superior Mesenteric aa
R+L renal aa
Inf Mesenteric aa
The ascending aorta gives rise to the _ arteries which supply blood to the _
coronary
heart
The _ aorta supplies blood to the chest wall, lungs, and esophagus
thoracic
The _ aorta supplies blood to the _ and pelvic organs, as well as lower limbs
abdominal
The A of A (artery of adam) supplies the _ (ant or post) _ (1/3 or 2/3) of the SC via the _ (ant or post) spinal arteries
anterior
2/3
anterior
Damage to the A or A can occur via surgical complications, trauma, or vascular dz. leading to SC _ -> _ or other serious neurological conditions (Beck’s SYNDROME - not triad)
SC ischemia -> paraplegia
The anterior 2/3 of the SC, which has arterial blood supply from the _ of _, is responsible for _ + _ function
Artery of adamkiwicz
motor + sensory function
There is higher risk clamping _ (above/below) renal arteries
above
The A of A originates between the _ - _ vertebra supplies the _ (upper/lower) 2/3 of the SC
TV8- TV12
lower
The A or A is the largest _ artery
radiculomedullary
-means it supplies blood to the SC
Atherosclerosis is _ + _
systemic + progressive
Most common cause of PVD =
atherosclerosis
-should suspect presence in coronary, cerebral, and renal arteries if present elsewhere
Atherosclerosis primarily affects _ (arteries/veins) due to plaque formation -> stenosis and possible occlusion
arteries
Plaque Formation process: (1/8)
Damage to the _ lining of vessels -> inflammation + vessel wall more permeable to _
endothelial
lipids
Plaque Formation process: (2/8)
_ cholesterol enters damaged endothelium and accumulates on arterial walls, which then _ and causes an inflammatory response
LDL
oxidizes
Plaque Formation 3/8
WBCs, especially _ go to the site of injury and change into _
monocytes
macrophages
Plaque Formation 4/8
Macrophages eat oxidized LDL particles and become _ cells, forming _ _
foam
fatty streaks
Plaque Formation 5/8
Foam cells release _ _, making smooth muscle cells migrate from deep layers of the arterial wall to the site of the fatty streak, which _ and thicken the wall
growth factors
proliferate
Plaque formation 6/8:
A cap made of _ forms on the fatty streak which stabilize it temporarily but then continues to degrade -> more _
collagen
inflammation
Plaque Formation 7/8:
As more foam cells, smooth muscle cells, and _ _ _ accumulate and cause more plaque, which may _ into the arterial lumen -> occlusion
extracellular matrix components
protrude
Plaque Formation 8/8:
In advanced stages the fibrous cap can _ from inflammation, exposing its core to the bloodstream, triggering formation of a _
rupture
thrombus
Risk Factors for Atherosclerosis (BOX 28.1 Nagelhout):
age
smoking
HTN
DM
Insulin resistance
obesity
family hx
physical inactivity
gender (M>F)
hyper/hypohomocysteinemia (high or low levels of total homocysteine in blood - B6,9,12)
Elevated CRP and elevated lipoprotein
High BG, hyperlipidemia
renal dz
2 most common LE vessels affected by atherosclerosis:
-superficial femoral artery
-popliteal artery
fem-pop bypass
Atherosclerosis tx classes:
-Lipid lowering agents (statins, fibrates, PCSK9 inhibitors)
-Antiplatelets (low dose ASA)
-AntiHTN (ACEi, ARBs, BB, CCB)
-Blood sugar control (metformin, insulin, SGLT2 inhibitors)
-Anti-inflammatory meds (colchicine)
Target HR for pt on BB therapy for HTN + atherosclerosis
HR goal 50-60
BB are great for pts with HTN and PVD that are high risk for:
ischemia + infarction
Pts who have had a AAA repair will see a _ fold decrease in cardiac morbidity with adequate _ blockade
10x
BB
BB are best started _ - _ before surgery
days-weeks
Periop BB started within 1 day or less before non-cardiac surgery prevents nonfatal MIs but increases risks for:
HoTN
CVA
bradycardia
death
Common BB seen for HTN + PVD:
atenolol
metoprolol
labetalol
propranolol
Benefits of statins for PVD:
-decreases progression/causes regression of plaque
-improved endothelial function
-reduced vascular inflammation
-cardioprotective
-improves graft patency
-limb salvage
-lowers lipid conc
ASA-should we give it?
-ASA does NOT lower risk of CV event perioperatively
-DOES increase bleed risk
-HOLD preop
ASA when should it be restarted after surgery?
2-8 days
Types of surgeries done by VASCULAR surgeon:
-stenting
-atherectomy
-bypass
-endarterectomy
-thrombolysis or thrombectomy
-open aneurysm repair
-endovascular aneurysm repair (EVAR)
-Vein procedures (sclerotherapy/vein ablations)
Which vascular cases may involve a laser?
vein ablation or atherectomy
Majority of M+M assoc with PVD is caused by _ _
cardiac events
_ is the most common causative factor in the mortality of pts having surgery for vaso-occlusive dz
atherosclerosis
If pt has PVD also assess for which other dz processes:
CAD
DM
aortic aneurysm
cerebral vascular dz
renal dz
DM with PVD = higher risk of _ and _ _
MI
wound infection
Hyperglycemia can exacerbate _ injury
neuro
-tight control for CEA + thoracic aortic procedures
Which types of vascular cases would you want very tight glucose control due to the risks of neuro injury and exacerbation risk from high BG?
CEA
anything thoracic aortic regions
check BG, consider insulin gtt
-if pt is not IDDM, recheck BG 30 mins later after giving insulin, not 1hr
Development of atherosclerosis occurs in 2 stages: _ and _ to _
injury
response to injury
“fatty streak” is made of which 2 types of cells? which layer of the artery do they sit?
macrophages and T lymphocytes
intima
The core of plaque is made of _ _ and is surrounded by smooth muscle cells and collagen
foam cells
4 MAJOR risk factors for atherosclerosis:
smoking
DM
age
fam hx
Term for atherosclerosis affecting limb or claudication with limb ischemia?
PVD
Why correct HTN gradually prior to surgery?
to allow for normalization of intravascular volume
Things to ask dialysis pt in preop:
-dialysis schedule + last appointment
-was fluid removed/how much
-what is their K!
-what kind of renal injury do they have
Clamping the aorta _ the renal arteries has the largest risk of injury because blood flow is decreased by _ % when done so
above (suprarenal clamp)
80% less renal BF
Hemodynamic changes don’t immediately reverse upon removal of aortic clamps and may last for at least _ min before return to baselien
30min
When should dialysis pt have dialysis in regard to surgery?
day before or DOS are ideal
Preop renal dz pts having vascular surgery, which labs do you want?
Baseline BUN + Creat, lytes (K!!!)
Possible patho of AKI in setting of vascular surgery:
renal IRI
-reperfusion ischemia/injury
nephrotoxic drugs
-ACEi, NSAIDs, aminoglycoside abx, diuretics
athero-embolization to renal arteries
T/F Introp UO is predictive of postop renal function
false!
Renal BF decreases:
-suprarenal aortic clamping
-infrarenal aortic clamping
supra: renal BF drops by 80%
infra: renal BF drops by 45%
Biggest concern with pt with carotid artery dz:
CVA risk
Surgical tx of SYMPTOMATIC carotid artery dz:
Carotid Endarterectomy (CEA)
Carotid Angioplasty and Stenting
Medical tx of ASYMPTOMATIC carotid artery dz:
-ASA
-plavix
-smoking cess
-anti HTN
-statins
-lifestyle changes (BRIEF-wt loss, diet, exercise, limit ETOH etc)
-follow ups!
Indications for CEA:
SYMPTOMATIC carotid stenosis
-hx TIA with 70-99% stenosis
-some cases 50-70% stenosis with high risk factors for CVA
ASYPTOMATIC carotid stenosis
-60-99% stenosis if in good health and <75yo
CEA is recommended within _ wks of a TIA to prevent further eventsd
2wks
Why is it important for us to know the percent stenosis on BOTH carotids before surgery?
tells us if there is collateral BF and helps us know how likely the pt will be needing a shunt during the case
S/S of carotid dz are usually caused by _
embolization
S/S of carotid dz:
amaurosis fugax (transient monocular vision loss = emergency)
paresthesia
clumsiness of extremities
speech issues
Primary NONINVASIVE test for carotid dz:
carotid duplex US
-grades, measures, monitors stenosis
sensitivity + specificity to detect stenosis >60% ~ 94% spec
Amaurosis Fugax is a medical emergency involving transient _ _ loss associated with _ artery dz
monocular vision loss
carotid
Amaurosis Fugax can be caused by:
embolism > retinal artery occlusion
-inflammation of nerves and arteries nearby
A carotid angiogram uses _ and _ _ injected into arteries in the arm or groin to visualize stenosis, blockages, or abnormalities.
XRay
contrast dye
The H+N region obtains most of its blood supply from the _ and _ arteries
carotid and vertebral
The _ arteries are the primary supply of blood to the brain and face
carotid
The R common carotid artery originates in the neck from the _ artery
brachiocephalic
The L common carotid artery originates in the neck from the:
aortic arch
Both R + L common carotid arteries bifurcate in the neck at the level of the _ _ into the _ and _ carotid arteries
carotid sinus
internal
external
What do these arteries supply:
-internal carotid
-external carotid
ICA: brain
ECA: neck + face
What is the green X?
common carotid artery
What is the green X?
internal carotid artery
What is the green X?
external carotid artery
What part of the internal carotid artery is the green X?
cervical part
What part of the internal carotid artery is the green X?
cerebral part
What part of the internal carotid artery is the green X?
petrous part
What part of the internal carotid artery is the green X?
cavernous part
The carotid arteries originate posterior to the _ joints in the neck
sternoclavicular joint
The carotid arteries are contained within the _ _ behind the _ musccle
carotid sheath
sternocleidomastoid mm
The common carotid arteries bifurcate in to the _ and _ at the _ border of the thyroid cartilage (~ _ or _ cervical vertebra)
ICA + ECA
upper
CV 4 or 5
Why is the bifurcation point of the common carotid artery clinically significant:
-location point for the carotid body chemoreceptor and the carotid sinus baroreceptor
This part of the carotid artery is sensitive to decreased PO2 , increased PCO2, and decreased blood pH and alerts the brain to change the RR:
carotid BODY CHEMORECEPTOR
-chemoreceptor = CHEMICAL changes - PO2,PCO2,pH > RR
This part of the carotid artery responds to changes in the stretch of the blood vessel and is responsible for detecting changes and maintaining BP
carotid SINUS BARORECEPTOR
-baroreceptor = PRESSURE changes > keep BP ok
The _ _ is the small dilated area found at the common carotid bifurcation where it becomes the ICA and ECA
carotid sinus
The carotid sinus, found at the bifurcation, contains _ which detect changes in BP
baroreceptors
-side note: surgeon will be tugging on this thing
Carotid Detection of BP changes: (1/3)
The _ in the carotid sinus are sensitive to stretch on the _ wall, corresponding with BP
baroreceptors
arterial
Carotid Detection of BP changes: (2/3)
When BP increases, the receptors stretch more, signaling to the brain (via the _ _) via the _ nerve (CN _)
medulla oblongata
glossopharyngeal - CNIX
Carotid Detection of BP changes: (3/3)
When BP drops, the signals from these receptors _
decrease
Role of carotid sinus in BP regulation:
high BP
brain reduces SNS activity and increases PSNS activity > slowed HR, vessels dilate > BP drops
Role of carotid sinus in BP regulation:
low BP
SNS activity is increased > vasoconstriction and increased HR > BP increases
_ _ is the brains intrinsic ability to maintain stable BF across ranges of BP, protecting it from ischemia or _
cerebral autoregulation
HYPERperfusion
Mechanism of autoregulation in brain:
vessels constrict or dilate in response to BP
-BP is low, vessels dilate to increase BF
_ (CPP/ CBF) can maintain relatively constant at different _ (CPP/CBF)bc of cerebrovascular autoregulation
CBF
CPP
CPP (cerebral) = _ - _
CPP = MAP - ICP
CBF remains constant at a MAP between:
60-150mmHg
Chronic HTN shifts the cerebrovascular autoreg curve to the _, requiring _ MAP to maintain CBF
right
higher
Pts with HTN, DM, or atherosclerosis may have a _ range of effectiveness of autoreg
narrower
What can occur during a CEA that disrupts autoregulation, risks ischemic events or reperfusion injury ?
carotid sinus manipulation temporarily or permanently disrupting baroreceptor function
During CEA, manipulation of the carotid _ can lead to transient or lasting _ dysfunction > labile BP
sinus
baroreceptor
Why is meticulous BP mgmt required during a CEA case?
bc cerebral autoreg can be compromised from messing with carotid sinus and cause labile BP > risk for ischemic or hyperperfusion events
-brain wont autoreg well so we have to
Anesthetic goals of a CEA case:
Hemodynamics:
-keep MAP higher (80-100; autoreg is shifted R)
-protect heart and brain from ischemic injury
-ask surgeon for ok BP range and know preop BP
-ablate surgical pain/stress responses!
Awake pt at end of case for neuro checks!
Know when to heparinize/protamine
-consider dextran to prevent anaphylactoid reaction from protamine
CEA prep:
-5 lead, watch ST changes
-RADIAL A LINE + BP CUFF on CONTRALAT ARM
-2 LARGE BORE IV (arms tucked)
-stopcock for gtts close to pt arm
-IVAC
-eye protection
-ACT machine / L + cuvettes
-pressors (phenyl, levo, ephedrine) and BP lowering agents (NTG, nipide, nicardipine)
When aorta clamping, keep ABP _ % above baseline for CEA
10%
Managing CEA challenges:
surgical manipulation of carotid sinus activates baroreceptor reflex and pt’s HR is low and HoTN, now what
-tell surgeon stop if possible
-infiltrate carotid bifurcation with 1% Lido (blunts reflex)
-ephedrine/phenylephrine
During CEA, “stump pressure” is the ICA back pressure and a pressure of < _ - _ mmHg = hypoperfusion (low collateral flow) and indicates need for a _
<40-50mmHg
shunt
Goal of shunt during CEA:
maintain CBF + decrease cerebral ischemia
-increases collateral flow with shunt
-decreases cerebral metabolic requirements
Things to avoid during a CEA case:
HoTN during cross clamp
HYPERcapnia (want 32-35) -> steal phenomenon
HYPERGLYCEMIA -brain swelling (LR v NS)
hypothermia (avoid bair hugger?)
CO2 is a potent _, which can _ CBF at high levels and also cause uneven blood distribution > worse ischemic conditions
VASODILATOR
increases
Higher CO2 levels can _ ICP, especially in patients with narrow autoreg > increased risk of cerebral edema and poor perfusion
increase
High CO2 can enhance the steal phenomenon which shunts blood _ _ already ischemic areas
away from
Gold standard of cerebral monitors for CEA cases =
awake, cooperative pt!
-will see change in grip strength or consciousness in ~2 min after clamping or shunting
-good with superficial cervical plexus block of C2-C4
Neuromonitoring options for CEA:
EEG
only see changes in 28% of CEA
-not very reliable, anesthesia interferes
-high false positives
-can tell risk of periop stoke
Neuromonitoring options for CEA:
16 channel strip
complex, tech needed
2-4 channel is easier to read, but less accurate
Neuromonitoring options for CEA:
SSEPs
can indicate subcortical ischemia but require a tech, high false positives, and need lighter anesthesia
Neuromonitoring options for CEA:
Transcranial doppler
assess hemodynamic ischemia, shunt function, embolic phenomenon, reperfusion syndrome
Neuromonitoring for CEA:
Cerebral oximetry
get baseline
-similar to pulse ox with near infrared light
-regional SO2 of <20% from preclamp to early cross clamp value has a high negative predictive value, AKA if rSO2 doesnt decrease more than 20% ichemia by hypoperfusion is NOT likely and a shunt should NOT be necessary
Purpose of heparin for CEA cases
prevent thromboembolic complications
How much heparin should you draw up for a CEA case?
10,000 units
-surgeon will order dose (100units/kg)
When to check ACT when giving heparin for CEA (Q!)
-baseline
-3-5 min after initial dose
-Q20-30 min
-after reversing protamine (make sure back to a normal/therapeutic level)
-use the low range (LR) cuvettes
What ACT level do we want before ICA clamping during a CEA?
250-375 sec
Who decides if pt needs a shunt for CEA?
surgeon
-ask during time out usually
Shunts are most often utilized during CEA surgery when:
there is severe BL carotid dz
It’s important to know the extent of dz in the _ carotid artery during a CEA
ipsilateral
CEA emergence:
-AWAKE with minimal coughing (precedex is great)
-resident holds pressure on neck to prevent straining
-neuro exam upon wake up
-AVOID excessive versed/benzos before or after
-turn IA off early to avoid delayed emergence
Gold standard technique for CEA:
regional + awake!
-superficial cervical plexus block C2-C4 dermatomes!!!!!!
-block done in preop
-prep pt for everything (tell them about drapes, laying still, any pressure or talking
Cervical plexus block technique:
inject at transverse process of C2, C3, and C4 at posterior border of the sternocleidomastoid muscle
Pros of Regional for CEA:
-better stability of BP
-easy cerebral monitoring
-avoid intubation
-less need for negative inotropes
-less episodes of EEG ischemia
-less costs
Cons of Regional for CEA:
-pt may panic
-sudden loss of consciousness
-seizures possibly
-airway control may be difficult (esp if mid procedure and neck is open)
-quality + timing of block may not be ideal
CEA postop management: risks
-neuro dysfunction
-hemodynamic instability
-respiratory insufficiency
-CN deficit
-hematoma
-hyperperfusion syndrome
Hyperperfusion syndrome can occur within _ to _ after a CEA
days-wks
What causes hyperperfusion syndrome?
restored BF > sudden increase in BP and flow to brain esp in area that were under-perfused; if BF regulation is disrupted (HTN after surgery) it can lead to hyperperfusion syndrome
Hyperperfusion syndrome s/s:
severe HA, N/V, confusion, vision changes, seizures, intracerebral hemorrhage
-these s/s look like a stroke (GO RIGHT TO CT!)
Hyperperfusion syndrome risk factors:
HTN after surgery (biggest one)
old age
poorly controlled preop HTN
previous hx of CVA or TIA
If a pt is very HTN postop after CEA, which medications might be good options?
Nipride
NTG
Common nerve injuries post-CEA
CN II Facial
CN IX Glossopharyngeal
CN X Vagus
CN XI Spinal Accessory
CN XII Hypoglossal
Signs of CN II injury:
asymmetric face movement
-smiling
Signs of CN IX injury:
impaired gag/ swallow on one sd
Signs of CN X injury:
hoarseness, uvula deviation, diminished palatal elevation
Signs of CN XI injury:
UL shoulder droop, weak head rotation against resistance
-cant shrug
Signs of CN XII injury:
tongue deviation to AFFECTED sd, reduced lateral tongue movements
Aortic aneurism vs aortic dissection
Aneurysm: bulge/dilation at weak part of aorta
-chest/ thorax(type A) or abdominal (type B)
Dissection: tear on inner layer of aortic wall, blood enters and forces layers apart, painful
Risk factor for aortic aneurysm:
Age (>65)
Gender (m >f)
Fam Hx
Smoking (higher risk for abdominal)
HTN
Atherosclerosis
Genetic disorders (Marfan syndrome, Ehlers-Danlos syndrome, Turner syndrome, Bicuspid valve))
Infections/Inflammation (can worsen)
Most abdominal aortic aneurysms are located _ the renal arteries
below
Most thoracic aortic aneurysms involve the _ _ and/or the _ aorta
aortic root
DESCENDING aorta
Aortic aneurysms are high risk for rupture at > _ cm diameter
> 5cm
Aortic aneurysm s/s:
most are asymptomatic
-palpation of abdomen on physical exam
pain in abdomen, chest, lower bain, or groin (indicative of possible impending rupture)
acute pain = possibly ruptured
Risk of aneurysm rupture is directly related to the _ _ of the aneurysm
luminal diameter
AAA represents dilation of the abdominal aorta _ the level of the renal arteries
BELOW
Risk of aortic aneruysm rupture increases when:
-aneurysm is >4.5-5cm diameter
-increases by a median of 0.3cm / yr
Theoretical basis for using “maximum diameter criterion” for AAA rupture prediction is what law?
LaPlace’s Law
-stress on AAA wall is proportional to diameter
What is LaPlace’s Law?
stress on wall of lumen is proportional to its diameter
(AAA)
Monitors/ tools needed for Open Aortic Repair:
-5 lead
-2x large bore IV (blood tubing)
-A line (dominant arm)
-central access / SG depending on CV dz
-TEE or PVV
-fluid warmers
-500mL pressure bags
-cell saver /hemocue
-NTG
-avoid HTN on induction + be gentle to avoid rupture (consider esmolol)
Open Aortic Surgery incision approach:
vertical anterior midline or retroperitoneal
Open Aortic Aneurysm Surgery
-technique
-anesthesia goals
GA
-keep warm
-keep HR slow (avoid tachy)
-avoid HTN or hypoperfusion
-anticipate high EBL
Induction for open AAA:
-goals
-drugs
Goals: hemodynamic stability, adequate depth anesthesia to reduce SNS response (avoid VS extremes), quick gentle intubation (GLIDE 1st)
Agents: etomidate (preferred), propofol (carefully), fentanyl/remifentanil (better bc precise control and quick on/off), Rocuronium
Why avoid N2O with open aortic repair surgery?
N2O can increase risk of bowel distention > increased intra-abdominal pressure > worsening conditions
Why give a fluid bolus before clamping in open aortic surgery?
to compensate for sudden drop in venous return about to happen
When is the best time to give fluids in open aortic aneurysm surgery?
RIGHT before clamping to increase preload bc venous return will drop
What do you want prepped BEFORE clamping?
NTG (or be ready to increase IA)
pt is heparinized (check ACT)
pt SLIGHTLY hypovolemic (despite lil fluid bolus?)
can give mannitol 0.5g/kg 30 min before clamping for renal protection
Issues when clamping aorta can be from:
-level (diff hemodynamic changes on diff areas)
-LV status
-degree of collateral circulation
-intravascular blood volume
-SNS activation
-response to anesthesia drugs/ technique
Which poses LESS risk for SCI: infrarenal aortic clamping or suprarenal?
infrarental
What happens hemodynamically when aorta is clamped?
HTN ABOVE the clamp
Intense HOTN BELOW (80% drop in MAP!)
Increased afterload, SVR, MAP, PAOP
CO normally DECREASES!
Increased O2 consumption/demand
blood volume redistributes (adjusts after ~15 min)
Goals DURING clamping for open aortic aneurysm repair:
Increased IVFs, blood, CS slowly until closer to unclamping
Monitor urine output Q 30 min (want 1mL/kg/hr)
Monitor ACT Q 30 min + adjust
Avoid hypovolemia (large 3rd space losses)
Crystalloids + blood: CS + PRBC expect 600mL-2L EBL
temp control
Prior to release of aortic cross clamp
-anesthesia goals
HEMODYNAMICS:
expect HOTN (blood rushing to previously ischemic areas)
volume loading (give boluses to help maintain preload after clamping-check with perfusionist to give back CS, have 500cc bags ready for boluses)
*Calcium administration (can counteract myocardial depression from reperfusion syndrome)
decrease IA and vasodilators (to avoid HOTN)
prep pressors (phenyl + levo) to treat HOTN
COMMUNICATE W SURGEON:
-can unclamp all at once or one leg at a time (have plans A,B, and C)
Post-release of aortic cross clamp
-declamping shock management
-watch for severe HOTN from volume redistribution (boluses and pressors, may be transient)
-manage acidosis and hyperK (from any anaerobic washout and vasodepressor substances from ischemic tissue) (bicarb, fluids, hyperventilation, inotropes)
-monitor hemodynamics and consider reclamping if bad enough (optimize CO and SVR)
Standard measures to prevent SCI during aorta surgery clamping
-shorten X clamp time
-maintain normal CO
-keep perfusion pressures higher
The A of A supplies the SC at the _ level mainly
thoracolumbar
Most (75% of cases) of the time, the A of A joins the _ (anterior/posterior) spinal artery at T _ - T _
anterior
T9-T12
Why could a SCI happen during vascular surgery?
interrupted BF to arteries supplying SC (like A of A) during cross clamping
-reduces distal MAP > reduced SC perfusion pressure
-clamping reduces perfusion to the SC -> ischemia and edema
Purpose of CSF drain during thoracoabdominal aortic surgery:
-minimize risk for SCI
-reduces CSF pressure and optimizes SC perfusion pressure and SC BF
-primary prevention and management in both thoracoabdominal aortic surgery or endovascular surgery
How do clamps in thoracoabdominal aortic surgery or endovascular surgery pose risk for SCI?
clamp increases CSF pressure and decreases distal aortic systolic pressure (past the clamp) > decreased perfusion pressure to SC
-CSF lumbar drain can help lessen pressure and improve blood flow to SC
Thoracic aortic ruptures are often caused by _ injuries
deceleration injuries (MVA)
Most (45%) of thoracic aortic aneurysms occur in the _ aorta
ascending
Most thoracic aortic aneurysms occur distal to the origin of the _ artery
subclavian
Which type of aneurysm is the most challenging?
thoracic aortic
Where do they clamp when clamping for a thoracic aortic aneurysm?
supraceliac
Anesthesia goals for thoracic aortic aneurysm surgery:
manage BP, avoid organ ischemia, treat comorbidities, control bleeding, depends on site of lesion
Complications and risks associated with aneurysm repair:
cardiac M+M
hemorrhage
renal fail
paraplegia
resp fail
MODS
LEFT VC paralysis
CVA
T/F the true lumen of the aorta is dilated during an aortic dissection
false, it is COMPRESSED
An aortic dissection is when blood penetrates the aortic _ and forms either an expanding hematoma (type _ ) or a false channel for flow between medial layers (type _), causing the TRUE lumen of the aorta to be _
intima
type A - hematoma
type B - false channel between layers
compressed
Dx testing for an aortic dissection:
EKG
CXR
CT/MRI
Angiography
TEE
Labs
Risk factors for aortic dissection:
male
age + 65
hx of HTN
Marfan Syndrome + Ehler Danlos (connective tissue dz)
Aortic Dissection Type A s/s
ANTERIOR cp
ripping/tearing sensation
CHF s/s from AR or narrowing of true lumen
-HTN initially is from pain, then HOTN from rupture into retroperitoneum, hemiparesis/hemiplegia from carotid artery involvement
may involve entire aorta (s/s of ascending and descending are present)
Aortic Dissection Type B dissection: s/s
BACK pain in high up region (midscapulr)
HTN from pain
may mimic acute abdomen
N/V
Bowel ischemia from compression or dissection of mesenteric or celiac artery
paraplegia possible from occlusion of A of A
Endovascular stenting is used to treat _ or also _
AAA
TAA
Endovascular aortic stenting
-preop concerns
similar to those of open AAA
need C-line??
similar decisions regarding invasive lines
EVAR vs OAR based on:
AAA size
AAA morphology
Pt perioperative status/risk
Endovascular stenting:
-anesthesia options
GA
Regional
LA
Considerations when converting from EVAR to OAR:
-difficult arterial access
-vessel dissection at arterial access site
-poor anatomy parameters for EVAR
(tortuous iliac arteries, stent malpositioning, stent migration, aneurysm rupture)
Complications of endovascular aortic stenting:
Endoleak (persistent BF out of wall of stent graft into aneurysm sac)
problem with arterial access
migration or mispositioning of stent (scarring “glues” it in)
contrast-induced nephropathy
aneurysm rupture
3 clinical indications for lower extremity revascularization
claudication
ischemic rest pain or ulceration
gangrene
T/F Flushing of the graft during grafting or thrombectomy can cause significant blood loss
true
Most stimulating part of the procedure for lower extremity revascularizations:
tunneling of the graft
Lower extremity revascularization anesthesia options:
GA (ETT/LMA) vs Regional
Benefits of regional anesthesia for lower extremity revascularization:
less blood loss
reduced DVT rates (sympathectomy induced vasodilation)
decreased N/V
negative intubation complications, AMS, cognitive dysfunction, or respiratory difficulties
improved pain control
What is a potential surgical emergency following lower extremity revascularization surgery?
acute arterial occlusion > risk for compartment syndrome
What is the main risk and potential considerations that are associated with acute arterial occlusion following lower exxtremity revascularization surgery?
potential for compartment syndrome
-check K levels
-myoglobin released (AKI risk)
-fasciotomy may be required
Vascular access procedures for dialysis:
Quinton
AV fistula
AV graft
1st choice option for vascular access for dialysis
AV fistula
Which dialysis access is places similar to a central line in urgent situations?
Quintons
Which dialysis access is the first choice, and is constructed with an end to side vein-artery anastamoses?
AV fistula
Which dialysis access option is a synthetic graft constructed by anastamosing artery and veins, straight or looped and will be more likely to require a thrombectomy?
AV graft
Anesthesia options for vascular access for dialysis
LMA or MAC/light sedation
Things to ask prior to vascular access surgery for dialysis:
- when was pt dialyized last, what is their schedule, and how much fluid was removed
-what is the K
-is pt hypovolemic or anemic at all?
-how is BP? (assume it will drop quickly)
Venous insufficiency procedures:
radiofrequency ablation
laser tx
foam sclerotherapy
microphlebectomy
