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N934 Adv Principles Fa 21 > Anesthesia for Vascular Surgery > Flashcards

Anesthesia for Vascular Surgery Flashcards

1
Q

common coexisting diseases with vascular patients include (6)

A

DM, HTN, renal impairment, pulmonary disease (r/t smoking), systemic atherosclerosis, CAD

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2
Q

leading cause of perioperative mortality at the time of vascular surgery?

A

CAD

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3
Q

pathology of atherosclerosis

A

generalized, progressive, chronic inflammatory DO of the arterial tree with development of fibrous intimal plaque associated endothelial dysfunction

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4
Q

what does atherosclerosis lead to when BF is compromised? (3)

A

MI, CVA, gangrene of LE’s.

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5
Q

atherosclerosis progression: stage 1, fatty streak

A

starts in childhood! enthothelium is damaged due to hemodynamic shear stress, oxidized LDL destruction, chronic inflammatory responses, infection, and hypercoagulability resulting in thrombosis. lipoproteins enter arterial intimal layer via endothelium. they become trapped. macrophages come, inflammation promoted. foam cells are formed

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6
Q

atherosclerosis progression: stage 2, fibrous plaque

A

composed of oxidized lipid accumulation, inflammatory cells, proliferated smooth muscle cells, connective tissue fibers, calcium deposits. blood flow reduction-ischemia to vital organs and extremities, thrombus risk

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7
Q

atherosclerosis progression: stage 3, advanced lesion

A

plaque with expanded lipid rich necrotic core, calcium accumulation, endothelial dysfunction. physical disruption of plaques protective cap (rupture or ulceration) exposes blood to highly thrombogenic material promoting acute thrombus formation and vasospasm. complete occlusion possible (MI, stroke, limb ischemia, etc)

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8
Q

atherosclerosis morbidity: three types

A
  1. enlarged plaque reduces limen of blood vessel. supply versus demand problem. can result in delayed periop MI (limb ischemia, stable angina)
  2. plaque rupture/ulceration/embolization, and thrombus formation. acute occlusion, can result in early periop MI (unstable angina, MI, TIA, CVA)
  3. Atrophy of media with arterial wall weakening (aneurysm dilation)
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9
Q

most common sites for atherosclerotic lesions

A

occurs at bifurcations

coronary artery and aortoiliac peripheral artery

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10
Q

2014 ACC and AHA preoperative evaluation guidelines include

A

clinical history (risk factors, exercise tolerance)
supplemental evaluation
perioperative therapy
surgical procedure itself (low risk, intermediate risk, high risk)

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11
Q

medical management and home meds: aspirin

A

inhibits platelets. increases bleeding and decreases GFR. continue for vascular procedures most of the time

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12
Q

medical management and home meds: plavix

A

inhibits platelets, potential increase in bleeding, do not continue on DOS

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13
Q

medical management and home meds: statins

A

effects liver function, continue on DOS

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14
Q

medical management and home meds: ACEI’s

A

induction hypotension, coughing, d/c 24h before surgery

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15
Q

medical management and home meds: diuretics

A

hypovolemia, electrolyte imbalance possible. continue DOS

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16
Q

medical management and home meds: CCB’s

A

HoTN is concern, continue on DOS

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17
Q

medical management and home meds: hypoglycemic drugs (and SE of one of them)

A

hypoglycemia, lactic acidosis with metformin. do not continue on DOS

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18
Q

medical management and home meds: BB’s.

A

bronchospasm, decrease in BP and decrease in HR. if you want to start them on a BB, start them 3-4d preop

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19
Q

post stenting and antiplatelet therapy

A

dual therapy will be required post stenting. usually ASA and plavix

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20
Q

when to stop anti platelet therapy for new bare metal stent

A

do not want to stop anti platelet therapy <1 month out from stent placement. usually on anti platelet therapy for 1-3 months

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21
Q

when to stop anti platelet therapy for drug eluding stent

A

do not want to stop anti platelet therapy <6 months out from surgery

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22
Q

critical period for coronary stenting

A

6 weeks to endothelialize

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23
Q

when performing a procedure on a previous coronary stent patient, what to do with preop ASA and plavix

A

continue ASA, hold plavix x7-8days

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24
Q

perioperative MI’s during vascular surgery are related to either

A 
culprit lesions (vulnerable plaques with high likelihood of thrombotic complications, often located in coronary vessels WITHOUT critical stenosis or
demand ischemia. this is likely the predominant cause and we can prevent this
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25
Q

tools and tests for cardiac function assessment for vascular surgery patients include

A
  • advanced cardiac testing to determine the need for coronary intervention prior to vascular surgery OR to determine if aggressive intraop/postop managment
  • exercise/ pharmacologic stress test
  • echo
  • assessment of ischemia, previous MI, valvular dysfunction, and heart failure
  • duplex imaging of carotid arteries or angiography (esp if sx of TIA’s)
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26
Q

most important pulmonary complications to assess for/risk of before vascular surgery include

A

atelectasis, PNA, ARF, exacerbation of underlying chronic disease

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27
Q

pulmonary tests to consider include

A

PFT’s, ABG’s, CXR’s

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28
Q

things to consider for patients with pulmonary dysfunction undergoing vascular surgery

A

incentive spirometry, steroids, regional, abx, CPAP

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29
Q

what strongly predicts long term mortality in patients with symptomatic LE arterial occlusive disease irrespective of disease severity, CV risk, and concomitant tx

A

chronic renal disease

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30
Q

preop tests to consider for renal function assessment

A

serum creatinine, creatinine clearance

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31
Q

things to consider for patients with renal dysfunction undergoing vascular surgery

A

contrast dye use, BB’s, statins, volume status, perfusion pressures

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32
Q

definition of LE PAD

A

insufficiency in LE’s presenting with acute or chronic limb ischemia with occlusions distal to the inguinal ligament

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33
Q

patients who need LE revascularization, often on what kind of meds?

A

ASA, ticagrelor (P2Y12 inhibitors), rivaroxaban (Xa inhibitor). clopidogrel
anti platelet and anticoagulant will likely both be on their regiment

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34
Q

peripheral revascularization indications

A 
acute ischemia (emboli, thrombus, pseudoaneurysm postop from femoral arterial line)
chronic ischemia (atherosclerotic plaque progressively narrowing vessel- claudication with eventual thrombosis of vessel)
35
Q

irreversible ischemic damage from acute ischemia occurs in how many hours

A

4-6 hours

36
Q

treatment for acute ischemic event

A

urgent thormbolytic therapy and/or angioplasty
arteriography
surgical intervention

37
Q

treatment for chronic ischemia: when is surgery indicated?

A

severe disabling claudication, critical limb ischemia (limb salvage)

38
Q

peripheral occlusions: traditional surgical approach for revascularization

A

unobstructed BF source (donor) artery is exposed. typical the common femoral, superficial, or deep femoral
target distal artery (recipient) is exposed at or below the knee. typically dorsals pedis or posterior tibial arteries
if saphenous vein used, vein is dissected all branches ligated, divided and excised (reversed, permits blood flow in direction of valves)
after donor and recipient arteries exposed, tunnel is created and graft is passed.
graft may be saphenous vein of prosthesis
heparin IV given (and not reversed)
anastomosis constructed
arteriogram to confirm adequate flow

39
Q

anesthetic managment of peripheral revascularization patient

A

preop BB’s and/or other chronic medication
intraop arterial line
continuous EKG monitoring and ST analysis (leads 2,5)
monitor intravascular volume by foley (+/- CVP or PA cath)
minimal blood loss and third spacing

40
Q

anesthetic management of peripheral revascularization patient for emergency surgery

A 
carefully watch K levels
myoglobinemia
fasciotomy may be required
coagulation status
EKG ischemia, etc
41
Q

anesthetic management of peripheral revascularization surgery: regional versus general

A

assess for coagulopathy or anticoagulation therapy
spinal may be best to avoid hematoma
regional superior to GA r/t to decrease in graft reocclusion
postop epidural versus PCA still a convo but PCA

42
Q

anesthetic management: cardiopulmonary complications and regional versus GA

A

no difference

43
Q

regional versus general: coagulation and BF

A

regional: promotes BF d/t sympathectomy
GA: hypercogulation more possible d/t decreased fibrinolysis

44
Q

postop: epidural versus opioids or PCA

A

postop epidural versus PCA still a convo but PCA seen more often

45
Q

epi, norepi, cortisol RA v GA

A

epi, norepi, cortisol release increased after GA compared to RA

46
Q

vasopressors and peripheral revascularization surgery

A

avoid vasopressors

47
Q

how to perform a GETA for peripheral revascularization surgery

A

opioids, inhlationals, N2O, NMB’s. deepen anesthetic during tunneling phase. ex) 3-5mcg/kg fentanyl. avoid hemodynamic extremes. BB’s often necessary

48
Q

how to perform regional anesthetic for peripheral revascularization surgery

A

L1-L4 dermatomes, T10 level adequate. epidural dosing usually 9-12mL including test dose. remember that elderly patients require decreased dosing

49
Q

postop anesthetic managment of patient after peripheral revascularization

A

control pain and anxiety (to decrease the risk of MI)
avoid anemia (HGB 9 or higher preferred)
control HR/BP
frequent checks of peripheral pulses
continuous EKG monitoring and ST analysis

50
Q

lower extremity endovascular treatment can be done as what type of anesthetic

A

GA, neuraxial, or MAC

percutaneous often MAC, open access (ex femoral stenosis) consider GA

51
Q

principal cause of carotid endarterectomy

A

atherosclerosis

52
Q

where does atherosclerosis often occur

A

common carotid, internal and external carotid arteries

53
Q

signs and symptoms of atherosclerosis occluding the carotids

A

fatal or debilitating CVA, TIA, amaurosis fogax aka transient monocular blindness, asymptomatic bruit

54
Q

leading risk factors of CVA (4)

A

DM, smoking, HTN, obesity

55
Q

indications for CEA (carotid endarterectomy)

A

patients with high grade carotid stenosis (70-99% occlusion) or that is symptomatic

56
Q

how to treat asymptomatic carotid stenosis

A

medical therapy (ASA), percutaneous angioplasty. usually

57
Q

preop assessment for CEA: medical management. how to optimize?

A

beta blockers, statins, anti platelet therapy.

HTN control, restore intravascular volume, reset cerebral auto regulation, DM control

58
Q

what is recommended before CABG?

A

carotid revascularization in patients with symptomatic carotid disease and bilateral severe asymptomatic carotid stenosis.

59
Q

anesthesia for CEA and lines

A

awake v GETA
aline always
PIVx2, arms usually tucked

60
Q

do you continue ASA for a CEA?

A

yes

61
Q

CEA and GA case setup includes (labs, lines, equipment, infusions, meds)

A

T&S
aline, act machine, fluid warmer, lower body forced air warming blanket
neo and remi infusions in line
clevidipine (1-2mg/h) and NTG (5-25mcg IV) infusions available
BB’s and ephedrine avail
heparin and protemine
esmolol during induction possible

62
Q

CEA and GA monitoring includes

A

routine with V5 lead and ST segment analysis plus aline
consider cerebral oximeter (foresight) esp if surgeons are not placing a shunt during cross clamp
occasionally surgeons want to measure “stump” pressures, so have an extra pressure tubing to connect to aline adapter

63
Q

can you use neo during CEA

A

yes because not a microvascular procedure

64
Q

where should the arterial blood pressure be maintained during a CEA

A

high-normal (~20%) for duration of procedure and especially during carotid clamping to increase collateral flow
(note pre induction MAP)

65
Q

what happens during surgical manipulation of the carotid sinus and how to treat it pharmacologically

A 
baroreceptor reflex (decrease HR and BP)
infiltration of carotid bifurcation with 1% lidocaine usually prevents further episodes.
66
Q

where are the baroreceptors located

A

aortic arch and internal carotids

67
Q

what happens if neurologic deficits are assessed during emergence from CEA

A

angiography, reoperation, or both

68
Q

emergence considerations for CEA

A

marked HTN and tachycardia can increase risk for ischemia and MI so tx aggressively and consider precedex/BB/something to smooth emergence

69
Q

regional anesthesia for CEA or “awake carotid” block

A

blocks C2 to C4 determatomes by use of superficial, intermediate, deep, or combined cervical plexus block

70
Q

benefits of awake carotid (regional anesthetic)

A

allows for continuous neurologic assessment for awake patient
reduces need for shunts
greater hemodynamic stability
reduced costs (avoid cerebral oximetry, dont need because theyre awake, and operative time is reduced)
requires patient cooperation

71
Q

describe a superficial cervical plexus block

A

locate the midpoint of the posterior border of the sternocleidomastoid muscle
injection along the posterior border of the medial surface of the muscle
may block accessory nerve causing trapezius muscle paralysis

72
Q

cerebral auto regulation: normal reactivity to hypocapnea

A

decrease in cerebral blood flow/vasoconstriction

73
Q

cerebral auto regulation: normal reactivity to hypercapnea

A

increase in cerebral blood flow/vasodilation

74
Q

what increases the risk for cerebral ischemia after carotid artery clamping

A

impaired CO2 reactivity (consider people with pulmonary diseases like COPD)

75
Q

describe the carotid artery stump pressure

A

ICA stump pressure represents back pressure resulting from collateral flow through circle of willis via contralateral carotid artery and vertebrobasilar system
may be performed every time or never performed

76
Q

what is the idea stump pressure

A

50 or greater

<45mmHg is cause for concern

77
Q

describe near infrared spectrophotometry

A

noninvasive technique that allows continuous monitoring of regional cerebral O2 saturation through the scalp and skull
based on oxygenated and deoxygenated HGB, however it measures O2 saturation of HGB of entire tissue bed and therefore approximates venous blood O2 saturation

78
Q

CEA postoperative complications

A

thromboembolic and hemorrhage intracerebral events
HTN r/t denervation of carotid sinus baroreceptors
HoTN r/t baroreceptor hypersensitivity
cerebral hyper-perfusion syndrome
cranial and cervical nerve dysfunction
carotid body denervation
wound hematoma
“loss of auto regulation once carotid is fixed”

79
Q

describe cerebral hyper perfusion syndrome (CEA postoperative complication)

A

abrupt increase in BF with loss of auto regulation manifested as HA, seizure, focal neurologic signs, brain edema, and possibly ICH

80
Q

describe types of cranial and cervical nerve dysfunction in relation to CEA postoperative complications

A

RLN, SLN, hypoglossal, mandibular

bilateral RLN injury and resultant bilateral vocal cord paralysis can result in life threatening upper AW obstruction

81
Q

describe carotid body denervation side effects in relation to CEA complications

A

impaired ventilatory response to mild hypoxemia, central chemoreceptors impaired, worsened with opioid administration

82
Q

steps to percutaneous transluminal angioplasty and stenting r/t endovascular carotid artery stenting

A

femoral access, aortic arch angiogram, selective cannulaiton of common carotid artery origin and angiogram, guide wire advancement into external carotid, sheath placement and advancement into CCA, placement of ambolic protection device, balloon angioplasty of lesion, advancement of stent delivery catheter across dilated lesion, deployment of self expanding stent, balloon dilation of stent, completion angiogram, access site management

83
Q

do patients who received percutaneous transluminal angioplasty and stenting need antiplatelet therapy

A

yes theyre on dual antiplatelet therapy

N934 Adv Principles Fa 21 (23 decks)

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