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NA 3 > Vascular PPT > Flashcards

Vascular PPT Flashcards

1
Q

Ascending aorta starts at the _ _ and ends at the _ _ (sternal angle ~ _ or _ rib)

A

aortic valve
aortic arch
2nd or 3rd rib

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2
Q

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.

A

arch of the ascending aorta
after
TV4

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3
Q

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).

A

Thoracic: aortic arch - diaphragm
-TV12

Abdominal: below the diaphragm – bifurcation of common iliac arteries
-LV4

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4
Q

The bifurcation of the aorta is at _ level which then splits into the R + L _ _ arteries

A

LV4
R+L common iliac

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5
Q

The 5 branches of the abdominal aorta before the bifurcation incluse:

A

celiac trunk
Superior Mesenteric aa
R+L renal aa
Inf Mesenteric aa

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6
Q

The ascending aorta gives rise to the _ arteries which supply blood to the _

A

coronary
heart

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7
Q

The _ aorta supplies blood to the chest wall, lungs, and esophagus

A

thoracic

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8
Q

The _ aorta supplies blood to the _ and pelvic organs, as well as lower limbs

A

abdominal

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9
Q

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

A

anterior
2/3
anterior

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10
Q

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)

A

SC ischemia -> paraplegia

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11
Q

The anterior 2/3 of the SC, which has arterial blood supply from the _ of _, is responsible for _ + _ function

A

Artery of adamkiwicz
motor + sensory function

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12
Q

There is higher risk clamping _ (above/below) renal arteries

A

above

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13
Q

The A of A originates between the _ - _ vertebra supplies the _ (upper/lower) 2/3 of the SC

A

TV8- TV12
lower

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14
Q

The A or A is the largest _ artery

A

radiculomedullary
-means it supplies blood to the SC

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15
Q

Atherosclerosis is _ + _

A

systemic + progressive

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16
Q

Most common cause of PVD =

A

atherosclerosis
-should suspect presence in coronary, cerebral, and renal arteries if present elsewhere

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17
Q

Atherosclerosis primarily affects _ (arteries/veins) due to plaque formation -> stenosis and possible occlusion

A

arteries

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18
Q

Plaque Formation process: (1/8)

Damage to the _ lining of vessels -> inflammation + vessel wall more permeable to _

A

endothelial
lipids

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19
Q

Plaque Formation process: (2/8)

_ cholesterol enters damaged endothelium and accumulates on _ walls, which then _ and causes an inflammatory response

A

LDL
arterial
oxidizes

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20
Q

Plaque Formation 3/8

WBCs, especially _ go to the site of injury and change into _

A

monocytes
macrophages

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21
Q

Plaque Formation 4/8

Macrophages eat oxidized LDL particles and become _ cells, forming _ _

A

foam
fatty streaks

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22
Q

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

A

growth factors
proliferate

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23
Q

Plaque formation 6/8:

A cap made of _ forms on the fatty streak which _ it temporarily but then continues to degrade -> more _

A

collagen
inflammation

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24
Q

Plaque Formation 7/8:

As more foam cells, smooth muscle cells, and _ _ _ accumulate and cause more plaque, which may _ into the arterial lumen -> occlusion

A

extracellular matrix components
protrude

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25
Q

Plaque Formation 8/8:

In advanced stages the fibrous cap can _ from inflammation, exposing its core to the bloodstream, triggering formation of a _

A

rupture
thrombus

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26
Q

Risk Factors for Atherosclerosis (BOX 28.1 Nagelhout):

A

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

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27
Q

2 most common LE vessels affected by atherosclerosis:

A

-superficial femoral artery
-popliteal artery

fem-pop bypass

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28
Q

Atherosclerosis tx classes:

A

-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)

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29
Q

Target HR for pt on BB therapy for HTN + atherosclerosis

A

HR goal 50-60

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30
Q

BB are great for pts with HTN and PVD that are high risk for:

A

ischemia + infarction

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31
Q

Pts who have had a AAA repair will see a _ fold decrease in cardiac morbidity with adequate _ blockade

A

10x
BB

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32
Q

BB are best started _ - _ before surgery

A

days-weeks

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33
Q

Periop BB started within 1 day or less before non-cardiac surgery prevents nonfatal MIs but increases risks for:

A

HoTN
CVA
bradycardia
death

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34
Q

Common BB seen for HTN + PVD:

A

atenolol
metoprolol
labetalol
propranolol

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35
Q

Benefits of statins for PVD:

A

-decreases progression/causes regression of plaque
-improved endothelial function
-reduced vascular inflammation
-cardioprotective
-improves graft patency
-limb salvage
-lowers lipid conc

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36
Q

ASA-should we give it?

A

-ASA does NOT lower risk of CV event perioperatively
-DOES increase bleed risk
-HOLD preop

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37
Q

ASA when should it be restarted after surgery?

A

2-8 days

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38
Q

Types of surgeries done by VASCULAR surgeon:

A

-stenting
-atherectomy
-bypass
-endarterectomy
-thrombolysis or thrombectomy
-open aneurysm repair
-endovascular aneurysm repair (EVAR)
-Vein procedures (sclerotherapy/vein ablations)

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39
Q

Which vascular cases may involve a laser?

A

vein ablation or atherectomy

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40
Q

Majority of M+M assoc with PVD is caused by _ _

A

cardiac events

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41
Q

_ is the most common causative factor in the mortality of pts having surgery for vaso-occlusive dz

A

atherosclerosis

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42
Q

If pt has PVD also assess for which other dz processes:

A

CAD
DM
aortic aneurysm
cerebral vascular dz
renal dz

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43
Q

DM with PVD = higher risk of _ and _ _

A

MI
wound infection

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44
Q

Hyperglycemia can exacerbate _ injury

A

neuro
-tight control for CEA + thoracic aortic procedures

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45
Q

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?

A

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

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46
Q

Development of atherosclerosis occurs in 2 stages: _ and _ to _

A

injury
response to injury

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47
Q

“fatty streak” is made of which 2 types of cells? which layer of the artery do they sit?

A

macrophages and T lymphocytes
intima

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48
Q

The core of plaque is made of _ _ and is surrounded by smooth muscle cells and collagen

A

foam cells

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49
Q

4 MAJOR risk factors for atherosclerosis:

A

smoking
DM
age
fam hx

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50
Q

Term for atherosclerosis affecting limb or claudication with limb ischemia?

A

PVD

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51
Q

Why correct HTN gradually prior to surgery?

A

to allow for normalization of intravascular volume

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52
Q

Things to ask dialysis pt in preop:

A

-dialysis schedule + last appointment
-was fluid removed/how much
-what is their K!
-what kind of renal injury do they have

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53
Q

Clamping the aorta _ the renal arteries has the largest risk of injury because blood flow is decreased by _ % when done so

A

above (suprarenal clamp)
80% less renal BF

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54
Q

Hemodynamic changes don’t immediately reverse upon removal of aortic clamps and may last for at least _ min before return to baselien

A

30min

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55
Q

When should dialysis pt have dialysis in regard to surgery?

A

day before or DOS are ideal

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56
Q

Preop renal dz pts having vascular surgery, which labs do you want?

A

Baseline BUN + Creat, lytes (K!!!)

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57
Q

Possible patho of AKI in setting of vascular surgery:

A

renal IRI
-reperfusion ischemia/injury

nephrotoxic drugs
-ACEi, NSAIDs, aminoglycoside abx, diuretics

athero-embolization to renal arteries

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58
Q

T/F Introp UO is predictive of postop renal function

A

false!

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59
Q

Renal BF decreases:
-suprarenal aortic clamping
-infrarenal aortic clamping

A

supra: renal BF drops by 80%
infra: renal BF drops by 45%

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60
Q

Biggest concern with pt with carotid artery dz:

A

CVA risk

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61
Q

Surgical tx of SYMPTOMATIC carotid artery dz:

A

Carotid Endarterectomy (CEA)

Carotid Angioplasty and Stenting

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62
Q

Medical tx of ASYMPTOMATIC carotid artery dz:

A

-ASA
-plavix
-smoking cess
-anti HTN
-statins
-lifestyle changes (BRIEF-wt loss, diet, exercise, limit ETOH etc)
-follow ups!

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63
Q

Indications for CEA:

A

SYMPTOMATIC carotid stenosis
-hx TIA with 70-99% stenosis
-some cases 50-70% stenosis with high risk factors for CVA

ASYPTOMATIC
-60-99% stenosis if in good health and <75yo

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64
Q

CEA is recommended within _ wks of a TIA to prevent further eventsd

A

2wks

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65
Q

Why is it important for us to know the percent stenosis on BOTH carotids before surgery?

A

tells us if there is collateral BF and helps us know how likely the pt will be needing a shunt during the case

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66
Q

S/S of carotid dz are usually caused by _

A

embolization

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67
Q

S/S of carotid dz:

A

amaurosis fugax (transient monocular vision loss = emergency)

paresthesia

clumsiness of extremities

speech issues

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68
Q

Primary NONINVASIVE test for carotid dz:

A

carotid duplex US
-grades, measures, monitors stenosis

sensitivity + specificity to detect stenosis >60% ~ 94% spec

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69
Q

Amaurosis Fugax is a medical emergency involving transient _ _ loss associated with _ artery dz

A

monocular vision loss
carotid

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70
Q

Amaurosis Fugax can be caused by:

A

embolism > retinal artery occlusion

-inflammation of nerves and arteries nearby

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71
Q

A carotid angiogram uses _ and _ _ injected into arteries in the arm or groin to visualize stenosis, blockages, or abnormalities.

A

XRay
contrast dye

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72
Q

The H+N region obtains most of its blood supply from the _ and _ arteries

A

carotid and vertebral

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73
Q

The _ arteries are the primary supply of blood to the brain and face

A

carotid

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74
Q

The R common carotid artery originates in the neck from the _ artery

A

brachiocephalic

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75
Q

The L common carotid artery originates in the neck from the:

A

aortic arch

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76
Q

Both R + L common carotid arteries bifurcate in the neck at the level of the _ _ into the _ and _ carotid arteries

A

carotid sinus
internal
external

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77
Q

What do these arteries supply:
-internal carotid
-external carotid

A

ICA: brain

ECA: neck + face

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78
Q

What is the green X?

A

common carotid artery

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79
Q

What is the green X?

A

internal carotid artery

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80
Q

What is the green X?

A

external carotid artery

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81
Q

What part of the internal carotid artery is the green X?

A

cervical part

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82
Q

What part of the internal carotid artery is the green X?

A

cerebral part

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83
Q

What part of the internal carotid artery is the green X?

A

petrous part

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84
Q

What part of the internal carotid artery is the green X?

A

cavernous part

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85
Q

The carotid arteries originate posterior to the _ joints in the neck

A

sternoclavicular joint

86
Q

The carotid arteries are contained within the _ _ behind the _ musccle

A

carotid sheath
sternocleidomastoid mm

87
Q

The common carotid arteries bifurcate in to the _ and _ at the _ border of the thyroid cartilage (~ _ or _ cervical vertebra)

A

ICA + ECA
upper
CV 4 or 5

88
Q

Why is the bifurcation point of the common carotid artery clinically significant:

A

-location point for the carotid body chemoreceptor and the carotid sinus baroreceptor

89
Q

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:

A

carotid BODY CHEMORECEPTOR

-chemoreceptor = CHEMICAL changes - PO2,PCO2,pH > RR

90
Q

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

A

carotid SINUS BARORECEPTOR

-baroreceptor = PRESSURE changes > keep BP ok

91
Q

The _ _ is the small dilated area found at the common carotid bifurcation where it becomes the ICA and ECA

A

carotid sinus

92
Q

The carotid sinus, found at the bifurcation, contains _ which detect changes in BP

A

baroreceptors
-side note: surgeon will be tugging on this thing

93
Q

Carotid Detection of BP changes: (1/3)

The _ in the carotid sinus are sensitive to stretch on the _ wall, corresponding with BP

A

baroreceptors
arterial

94
Q

Carotid Detection of BP changes: (2/3)

When BP increases, the receptors stretch more, signaling to the brain (via the _ _) via the _ nerve (CN _)

A

medulla oblongata
glossopharyngeal - CNIX

95
Q

Carotid Detection of BP changes: (3/3)

When BP drops, the signals from these receptors _

A

decrease

96
Q

Role of carotid sinus in BP regulation:
high BP

A

brain reduces SNS activity and increases PSNS activity > slowed HR, vessels dilate > BP drops

97
Q

Role of carotid sinus in BP regulation:
low BP

A

SNS activity is increased > vasoconstriction and increased HR > BP increases

98
Q

_ _ is the brains intrinsic ability to maintain stable BF across ranges of BP, protecting it from ischemia or _

A

cerebral autoregulation
HYPERperfusion

99
Q

Mechanism of autoregulation in brain:

A

vessels constrict or dilate in response to BP
-BP is low, vessels dilate to increase BF

100
Q

_ (CPP/ CBF) can maintain relatively constant at different _ (CPP/CBF)bc of cerebrovascular autoregulation

A

CBF
CPP

101
Q

CPP (cerebral) = _ - _

A

CPP = MAP - ICP

102
Q

CBF remains constant at a MAP between:

A

60-150mmHg

103
Q

Chronic HTN shifts the cerebrovascular autoreg curve to the _, requiring _ MAP to maintain CBF

A

right
higher

104
Q

Pts with HTN, DM, or atherosclerosis may have a _ range of effectiveness of autoreg

A

narrower

105
Q

What can occur during a CEA that disrupts autoregulation, risks ischemic events or reperfusion injury ?

A

carotid sinus manipulation temporarily or permanently disrupting baroreceptor function

106
Q

During CEA, manipulation of the carotid _ can lead to transient or lasting _ dysfunction > labile BP

A

sinus
baroreceptor

107
Q

Why is meticulous BP mgmt required during a CEA case?

A

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

108
Q

Anesthetic goals of a CEA case:

A

Keep MAP higher (80-100), autoreg shifted R
-protect heart and brain from ischemic injury
-ask surgeon for ok BP range
-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

Block baroreceptors when appropriate?

109
Q

CEA prep:

A

-5 lead, watch ST changes
-RADIAL A LINE + NIBP 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)

110
Q

When aorta clamping, keep ABP _ % above baseline for CEA

A

10%

111
Q

Managing CEA challenges:
surgical manipulation of carotid sinus > activated baroreceptor reflex > low HR and HoTN

A

-tell surgeon stop if possible
-infiltrate carotid bifurcation with 1% Lido (blunts reflex)
-ephedrine/phenylephrine

112
Q

During CEA, “stump pressure” is the ICA back pressure and a pressure of < _ - _ mmHg = hypoperfusion (low collateral flow) and indicates need for a _

A

<40-50mmHg
shunt

113
Q

Goal of shunt during CEA:

A

maintain CBF + decrease cerebral ischemia
-increases collateral flow with shunt
-decreases cerebral metabolic requirements

114
Q

Things to avoid during a CEA case:

A

HoTN during cross clamp
HYPERcapnia (32-35) -> steal phenomenon
HYPERGLYCEMIA -brain swelling (LR v NS)
hypothermia (avoid bair hugger?)

115
Q

CO2 is a potent _, which can _ CBF at high levels and also cause uneven blood distribution > worse ischemic conditions

A

VASODILATOR
increases

116
Q

Higher CO2 levels can _ ICP, especially in patients with narrow autoreg > increased risk of cerebral edema and poor perfusion

A

increase

117
Q

High CO2 can enhance the steal phenomenon which shunts blood _ _ already ischemic areas

A

away from

118
Q

Gold standard of cerebral monitors for CEA cases =

A

awake, cooperative pt!
-will see change in grip strength or consciousness in ~2 min after clamping or shunting

119
Q

Neuromonitoring options for CEA:
EEG

A

only see changes in 28% of CEA
-not very reliable, anesthesia interferes
-high false positives
-can tell risk of periop stoke

120
Q

Neuromonitoring options for CEA:
16 channel strip

A

complex, tech needed
2-4 channel is easier to read, but less accurate

121
Q

Neuromonitoring options for CEA:
SSEPs

A

can indicate subcortical ischemia but require a tech, high false positives, and need lighter anesthesia

122
Q

Neuromonitoring options for CEA:
Transcranial doppler

A

assess hemodynamic ischemia, shunt function, embolic phenomenon, reperfusion syndrome

123
Q

Neuromonitoring for CEA:
Cerebral oximetry

A

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

124
Q

Purpose of heparin for CEA cases

A

prevent thromboembolic complications

125
Q

How much heparin should you draw up for a CEA case?

A

10,000 units
-surgeon will order dose (100units/kg)

126
Q

When to check ACT when giving heparin for CEA

A

-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

127
Q

What ACT level do we want before ICA clamping during a CEA?

A

250-375 sec

128
Q

Who decides if pt needs a shunt for CEA?

A

surgeon
-ask during time out usually

129
Q

Shunts are most often utilized during CEA surgery when:

A

there is severe BL carotid dz

130
Q

It’s important to know the extent of dz in the _ carotid artery during a CEA

A

ipsilateral

131
Q

CEA emergence:

A

-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

132
Q

Gold standard technique for CEA:

A

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

133
Q

Cervical plexus block technique:

A

inject at transverse process of C2, C3, and C4 at posterior border of the sternocleidomastoid muscle

134
Q

Pros of Regional for CEA:

A

-better stability of BP
-easy cerebral monitoring
-avoid intubation
-less need for negative inotropes
-less episodes of EEG ischemia
-less costs

135
Q

Cons of Regional for CEA:

A

-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

136
Q

CEA postop management: risks

A

-neuro dysfunction
-hemodynamic instability
-respiratory insufficiency
-CN deficit
-hematoma
-hyperperfusion syndrome

137
Q

Hyperperfusion syndrome can occur within _ to _ after a CEA

A

days-wks

138
Q

What causes hyperperfusion syndrome?

A

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

139
Q

Hyperperfusion syndrome s/s:

A

severe HA, N/V, confusion, vision changes, seizures, intracerebral hemorrhage
-these s/s look like a stroke (GO RIGHT TO CT!)

140
Q

Hyperperfusion syndrome risk factors:

A

HTN after surgery (biggest one)
old age
poorly controlled preop HTN
previous hx of CVA or TIA

141
Q

If a pt is very HTN postop after CEA, which medications might be good options?

A

Nipride
NTG

142
Q

Common nerve injuries post-CEA

A

CN II Facial
CN IX Glossopharyngeal
CN X Vagus
CN XI Spinal Accessory
CN XII Hypoglossal

143
Q

Signs of CN II injury:

A

asymmetric face movement
-smiling

144
Q

Signs of CN IX injury:

A

impaired gag/ swallow on one sd

145
Q

Signs of CN X injury:

A

hoarseness, uvula deviation, diminished palatal elevation

146
Q

Signs of CN XI injury:

A

UL shoulder droop, weak head rotation against resistance
-cant shrug

147
Q

Signs of CN XII injury:

A

tongue deviation to AFFECTED sd, reduced lateral tongue movements

148
Q

Aortic aneurism vs aortic dissection

A

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

149
Q

Risk factor for aortic aneurysm:

A

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)

150
Q

Most abdominal aortic aneurysms are located _ the renal arteries

A

below

151
Q

Most thoracic aortic aneurysms involve the _ _ and/or the _ aorta

A

aortic root
DESCENDING aorta

152
Q

Aortic aneurysms are high risk for rupture at > _ cm diameter

A

> 5cm

153
Q

Aortic aneurysm s/s:

A

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

154
Q

Risk of aneurysm rupture is directly related to the _ _ of the aneurysm

A

luminal diameter

155
Q

AAA represents dilation of the abdominal aorta _ the level of the renal arteries

A

BELOW

156
Q

Risk of aortic aneruysm rupture increases when:

A

-aneurysm is >4.5-5cm diameter
-increases by a median of 0.3cm / yr

157
Q

Theoretical basis for using “maximum diameter criterion” for AAA rupture prediction is what law?

A

LaPlace’s Law
-stress on AAA wall is proportional to diameter

158
Q

What is LaPlace’s Law?

A

stress on wall of lumen is proportional to its diameter
(AAA)

159
Q

Monitors/ tools needed for Open Aortic Repair:

A

-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)

160
Q

Open Aortic Surgery incision approach:

A

vertical anterior midline or retroperitoneal

161
Q

Open aortic surgery anesthesia technique:

A

GA
-keep warm
-keep HR slow (avoid tachy)
-avoid HTN or hypoperfusion
-anticipate high EBL

162
Q

Induction for open AAA:

A

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

163
Q

Why avoid N2O with open aortic repair surgery?

A

N2O can increase risk of bowel distention > increased intra-abdominal pressure > worsening conditions

164
Q

Why give a fluid bolus before clamping in open aortic surgery?

A

to compensate for sudden drop in venous return about to happen

165
Q

When is the best time to give fluids in open aortic aneurysm surgery?

A

RIGHT before clamping to increase preload bc venous return will drop

166
Q

What do you want prepped BEFORE clamping?

A

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

167
Q

Issues when clamping aorta can be from:

A

-level (diff hemodynamic changes on diff areas)
-LV status
-degree of collateral circulation
-intravascular blood volume
-SNS activation
-response to anesthesia drugs/ technique

168
Q

Which poses LESS risk for SCI: infrarenal aortic clamping or suprarenal?

A

infrarental

169
Q

What happens hemodynamically when aorta is clamped?

A

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)

170
Q

Goals during clamping for open aortic aneurysm repair:

A

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

171
Q

Prior to release of aortic cross clamp:

A

-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)

172
Q

Post-release of aortic cross clamp:

A

Risk for declamping shock :
-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)

173
Q

Standard measures to prevent SCI during aorta surgery clamping

A

-shorten X clamp time
-maintain normal CO
-keep perfusion pressures higher

174
Q

The A of A supplies the SC at the _ level mainly

A

thoracolumbar

175
Q

Most (75% of cases) of the time, the A of A joins the _ (anterior/posterior) spinal artery at T _ - T _

A

anterior
T9-T12

176
Q

Why could a SCI happen during vascular surgery?

A

-interrupted BF to arteries supplying SC
-cross clamping

reduces distal MAP > reduced SC perfusion pressure

-clamping reduces perfusion to the SC > ischemia and edema

177
Q

Purpose of CSF drain during thoracoabdominal aortic surgery:

A

-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

178
Q

How do clamps in thoracoabdominal aortic surgery or endovascular surgery pose risk for SCI?

A

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

179
Q

Thoracic aortic ruptures are often caused by _ injuries

A

deceleration injuries (MVA)

180
Q

Most (45%) of thoracic aortic aneurysms occur in the _ aorta

A

ascending

181
Q

Most thoracic aortic aneurysms occur distal to the origin of the _ artery

A

subclavian

182
Q

Which type of aneurysm is the most challenging?

A

thoracic aortic

183
Q

Where do they clamp when clamping for a thoracic aortic aneurysm?

A

supraceliac

184
Q

Anesthesia goals for thoracic aortic aneurysm surgery:

A

manage BP, avoid organ ischemia, treat comorbidities, control bleeding, depends on site of lesion

185
Q

Complications and risks associated with aneurysm repair:

A

cardiac M+M
hemorrhage
renal fail
paraplegia
resp fail
MODS
LEFT VC paralysis
CVA

186
Q

T/F the true lumen of the aorta is dilated during an aortic dissection

A

false, it is COMPRESSED

187
Q

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 _

A

intima
type A - hematoma
type B - false channel between layers

compressed

188
Q

Dx testing for an aortic dissection:

A

EKG
CXR
CT/MRI
Angiography
TEE
Labs

189
Q

Risk factors for aortic dissection:

A

male
age + 65
hx of HTN
Marfan Syndrome + Ehler Danlos (connective tissue dz)

190
Q

Aortic Dissection Type A s/s

A

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)

191
Q

Aortic Dissection Type B dissection: s/s

A

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

192
Q

Endovascular stenting is used to treat _ or also _

A

AAA
TAA

193
Q

Endovascular aortic stenting
-preop concerns

A

similar to those of open AAA

need C-line??

similar decisions regarding invasive lines

194
Q

EVAR vs OAR based on:

A

AAA size

AAA morphology

Pt perioperative status/risk

195
Q

Endovascular stenting:
-anesthesia options

A

GA

Regional

LA

196
Q

Considerations when converting from EVAR to OAR:

A

-difficult arterial access

-vessel dissection at arterial access site

-poor anatomy parameters for EVAR
(tortuous iliac arteries, stent malpositioning, stent migration, aneurysm rupture)

197
Q

Complications of endovascular aortic stenting:

A

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

198
Q

3 clinical indications for lower extremity revascularization

A

claudication

ischemic rest pain or ulceration

gangrene

199
Q

T/F Flushing of the graft during grafting or thrombectomy can cause significant blood loss

A

true

200
Q

Most stimulating part of the procedure for lower extremity revascularizations:

A

tunneling of the graft

201
Q

Lower extremity revascularization anesthesia options:

A

GA (ETT/LMA) vs Regional

202
Q

Benefits of regional anesthesia for lower extremity revascularization:

A

**less blood loss

reduced DVT rates (sympathectomy induced vasodilation)**

decreased N/V

negative intubation complications, AMS, cognitive dysfunction, or respiratory difficulties

improved pain control

203
Q

What is a potential surgical emergency following lower extremity revascularization surgery?

A

acute arterial occlusion > risk for compartment syndrome

204
Q

What is the main risk and potential considerations that are associated with acute arterial occlusion following lower exxtremity revascularization surgery?

A

potential for compartment syndrome

-check K levels
-myoglobin released (AKI risk)
-fasciotomy may be required

205
Q

Vascular access procedures for dialysis:

A

Quinton
AV fistula
AV graft

206
Q

1st choice option for vascular access for dialysis

A

AV fistula

207
Q

Which dialysis access is places similar to a central line in urgent situations?

A

Quintons

208
Q

Which dialysis access is the first choice, and is constructed with an end to side vein-artery anastamoses?

A

AV fistula

209
Q

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?

A

AV graft

210
Q

Anesthesia options for vascular access for dialysis

A

LMA or MAC/light sedation

211
Q

Things to ask prior to vascular access surgery for dialysis:

A
  • 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)

212
Q

Venous insufficiency procedures:

A

radiofrequency ablation

laser tx

foam sclerotherapy

microphlebectomy

NA 3 (8 decks)

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